Factors that affect and influence industrial symbiosis (IS) collaborations have been researched extensively in the literature, where they are mostly reported at a network level or for IS in general, and lack the individual actor's perspective. This review article contributes to and expands knowledge of influencing factors and their effect on the individual actor. In a systematic review, guided by the PRISMA 2020 guidelines, this study reviews 53 scientific papers examining planned or existing IS networks. It examines literature from 1 January 2000 to 28 March 2022, and it identifies drivers, barriers, and enablers influencing actors to participate in IS. It explores whether and how the perception and impact of these factors differs depending on the characteristics of individual actors and their specific context. The main findings of this study reveal that an actor's specific characteristics and the network's context have a significant impact on decision making and how actors both perceive and are affected by factors influencing collaboration. Furthermore, an additional novel contribution to this field of research is that the study identifies three underlying and recurring considerations that actors appear to find critical, namely, perceived business opportunities/risks, regulatory and political setting, and potential inequalities in the network. The results show that an actor's take on these critical considerations determines whether the actor is willing to engage in IS.
A healthy working life is fundamental for individuals and society. To date, increasingly research connects the earlier, pre-working life to later working life experiences and beyond, recognizing that a worker's health and exposure starts before the working life begins. The research, however, often lacks a fundamental understanding of (i) the underlying mechanisms and pathways accounting for differences in different life stages and (ii) the role of the social environment in shaping working life experiences. By integrating a life course perspective in our research and crossing disciplinary borders in rigorous, collaborative research, we may get a better understanding of the complex and dynamic interplay between work, environment and health. A life course perspective for work environment and health research A life course perspective in work environment and health research emphasizes the importance of prior life experiences, including the environments in which individuals were raised and exposed, their familial and educational backgrounds, and their physical and mental health status before entering the workforce (1, 2). Life course research in different disciplines has been instrumental in developing more robust causal models (3, 4), particularly for understanding developmental health trajectories and socioeconomic health inequalities (eg, 5–7). Adopting an interdisciplinary life course perspective in work environment and health research helps researchers answering questions as to whether and how the timing, duration, intensity, and context of past and present exposures (ie, pre-working, working, and non-working exposures) are associated with later life work and health outcomes. For instance, the 'exposome paradigm' is a concept used to describe the sum of occupational and environmental exposures an individual encounters throughout life, and how these exposures impact biology and health (8). In exposome research, a broad range of genetic, biological, chemical, physical, social and lifestyle factors is examined throughout the life course to provide a comprehensive picture of potential risk factors impacting working life health (9). In exposome research and beyond, it is important to examine how the exposure-outcome relationships are shaped by specific social, cultural and historical contexts (2). The conceptual framework of the 'Social Exposome' may help to integrate the social environment in conjunction with the physical environment into the exposome concept (10). Moreover, focusing on both historical and contemporary contexts is essential not only for advancing research but also for informing policy and practice, for example by identifying entry points for interventions. Exposures during the life course During the individual's life course, several vulnerable time windows for the impact of a multitude of exposures that potentially harm, protect or promote health, eg, occupational, environmental and social, can be distinguished. The (combinations of) exposures may operate in different life stages and contexts and – directly or indirectly via intergenerational transmission – contribute to health (figure 1). The individual may be particulary sensitive to harmful exposures or adverse experiences during developmental life stages, ie, pre/perinatal, childhood, adolescence, pregnancy and menopause/andropause. Other life stages may reflect vulnerable time windows due to a clustering of exposures, eg, work and family demands during parenthood, or an accumulation of exposures during the (working) life course at retirement and post-retirement age. As illustrated in figure 1, occupational exposure(s) can be divided in exposure through the parents' exposure (early in life) and an individuals' own exposure (later in life). Already in the pre/perinatal life stage, occupational exposure starts through the intergenerational transmission of the parents' occupational exposures. Current and bioaccumulated occupational exposure of chemicals and particles in the father at the time of conception can affect sperm quality. Together with the mother's exposure to occupational exposures of chemicals and particles prior to conception – or chemicals, particles, physical factors, ergonomic load, organizational and (psycho-)social conditions at work during pregnancy – this may affect fetal development and later disease development during the child's life course (11–15). During childhood, the growing child is exposed to parental occupational exposure(s), directly through chemicals and particles in the work clothes and skin or indirectly through organizational and psychosocial factors in the work environment that may increase the risk for mental and physical health problems in parents, which in turn may affect their parental rearing quality (16, 17). During adolescence and early adulthood, individuals usually encounter their first direct occupational exposures through their first (student) job or jobs. Already from this life stage, occupational exposures may accumulate during the (working) life course and may affect not only the active working life but also the post working life. Also important to note is that brain plasticity is not limited to childhood, adolescence or young adulthood as it persists throughout life. Some studies indicate that high physical and chemical exposure during this life stage, can increase the risk of disease later in life (18). A poor psychosocial school or work environment in younger years may also increase the risk of adverse labour market outcomes and mental health problems later in life (19, 20). In adulthood, men and women often start with (the planning of) family formation. Some occupational exposures affect fecundability, others can increase the risk of pregnancy-related disease, such as preeclampsia, hypertension or diabetes, or affect the offspring (21, 22). Chemicals, heat and stress-related exposures affect the ability to conceive. During pregnancy, the bodily and mental systems are vulnerable with changes in the endocrine and inflammation response that can dysregulate the HPA-axis, resulting in a prolonged stress response. The placenta can filter out many hazards, but not all toxicants, such as methylmercury and arsenic (23, 24). Physical exposure, such as noise and vibration, but also shift and night work can affect the womb and cause fetal growth restriction, preterm birth, and hearing impairment (eg, 12, 13, 25–27). During parenthood, occupational exposures may affect the parents' (mental) health and work-family balance (28, 29). Many chemical and physical exposures have now manifested in disease, eg, allergy, asthma and musculoskeletal diseases (28). During menopause in women, with a drastic decrease in oestrogen, and the slow testosterone decline in men (sometimes referred to as andropause), dysregulations of the hormone system may disrupt and affect the individual's susceptibility for occupational exposures in a way similar to environmental exposures (30). Towards retirement, the total cumulative occupational exposure burden over the working life course and the current exposure will affect the ability to stay at work and in the labor market. Post retirement, most direct occupational exposures have ceased, but others may have (bio-) accumulated over time and may cause health problems that manifest after retirement (31, 32). Along with occupational exposures, a multitude of other exposures are present during the entire life course that may operate across different contexts to contribute to health (see figure 1). For instance, chemical, physical and social stressors during the life course leave traces ('memories') on the molecular and tissue levels that may affect later life health (33). Epigenetic marks act as heritable memories in the cell as they respond to different endogenous and exogenous signals and can be propagated from one generation of cells to the next generation of cells (33). Next to the epigenetic marks, the social environment and social determinants of health during the life course, eg, socio-economic and lifestyle factors, social relationships, social cohesion and support, are known to impact health and add to the multitude of exposures to be examined, among others in conjunction with the environmental exposome (eg, 34). In residential, family and school contexts, exposures such as air pollution, drinking water pollution, noise, artificial light at night, limited access to green space and crowding may play a role, as can adverse childhood experiences (eg, 35, 36). Moreover, on the overarching societal context, legislations, labor market conditions, norms, values and cultural aspects may affect worker health (2, 37). Main knowledge gaps and challenges Both conceptual and empirical challenges have to be tackled when conducting work environment and health research with an interdisciplinary life course perspective. On the conceptual level, different paradigms and nomenclature still exist in the various disciplines examining the impact of (occupational) exposures on later life health outcomes, which contributes to fragmented research and publication thereof in specialized journals. On the empirical level, questions arise such as: Is it feasible to examine mechanisms and pathways across different exposure levels considering a life course perspective? Is the follow-up duration of existing birth and other cohorts sufficient to address the dynamic interplay between the work environment and health? Are the multifaceted, constantly changing contexts captured? Effect sizes are often small on an individual level and statistical power decreases when several rare assumptions have to be fulfilled to examine clusters or combinations of exposures and contexts in relation to health outcomes. Big data, interdisciplinary research protocols and innovative, advanced statistical models to capture the life course perspective are needed to proceed beyond the exposome studies that are currently being finalized within the EU Horizon 2020 exposome call (https://www.humanexposome.eu). Moreover, a better understanding is needed of how occupational, environmental and social exposures affect individuals (i) in vulnerable time windows, eg, do exposures contribute to health advantages and/or disadvantages, and (ii) while transitioning between and within different life stages (38). Studies in different disciplines have focused on the childhood and retirement life stages, see eg, the research on the school-to-work transition or the work-to-retirement transition (39–41), but little is known about the menopause or andropause life stage. Last, rigorous examinations of different lifecourse models (eg, sensitive periods) and exposure models (eg, current, first, last, peak, single, chronic or accumulated), and their impact on health are needed within and across the different vulnerable time windows and life stages as exposure-outcome relationships may differ and thus call for targeted (preventive) policies and practices (42–44). Interdisciplinary research opportunities The challenges towards a better understanding of the complex and dynamic interplay between the work environment and health provide ample opportunities for rigorous, collaborative quantitative and in-depth qualitative life course research across different research strands. Researchers from different disciplines, such as occupational and environmental medicine, epidemiology, toxicology, health science, sociology, psychology, demography, public (mental) health, and genetics to name a few, should not shy away from the complexity, but embrace the opportunity to use their knowledge and skills to collectively address relevant research questions. Interdisciplinary research opportunities are already present today and will emerge even more in the years to come as more cohorts designed as birth cohorts or multi-generational cohorts mature (eg, LifelinesNext, 45). Researchers have or get access to (national) registers, databases with individual-level internal and external exposure information and neighbourhood-level exposure information or linkages of all these exposure and health data, allowing them to examine the impact of exposures in advanced causal models on later life health. To illustrate the value of and research opportunities with existing data, Ubalde-Lopez and colleagues (46) recently argued that parental work-related data collected in birth cohorts is a valuable yet underutilized resource that could be exploited more fruitfully in the collaboration between birth cohort research, occupational epidemiology and sociology. Having said that, the authors also refer to the possible constraints of eg, cross-national comparative research in terms of technical (ie, harmonization) and ethical challenges (46). In conclusion, to move research on the work environment and health forward, we call for a more integrated, interdisciplinary approach that considers the timing and accumulation of occupational, environmental and social exposures over the life course.
Background: Results on the association between prenatal exposure to methylmercury (MeHg) and child neuropsychological development are heterogeneous. Underlying genetic differences across study populations could contribute to this varied response to MeHg. Studies in Drosophila have identified the cytochrome p450 3A (CYP3A) family as candidate MeHg susceptibility genes. Objectives: We evaluated whether genetic variation in CYP3A genes influences the association between prenatal exposure to MeHg and child neuropsychological development. Methods: The study population included 2639 children from three birth cohort studies: two subcohorts in Seychelles (SCDS) (n = 1160, 20 and 30 months of age, studied during the years 2001–2012), two subcohorts from Spain (INMA) (n = 625, 14 months of age, 2003–2009), and two subcohorts from Italy and Greece (PHIME) (n = 854, 18 months of age, 2006–2011). Total mercury, as a surrogate of MeHg, was analyzed in maternal hair and/or cord blood samples. Neuropsychological development was evaluated using Bayley Scales of Infant Development (BSID). Three functional polymorphisms in the CYP3A family were analyzed: rs2257401 (CYP3A7), rs776746 (CYP3A5), and rs2740574 (CYP3A4). Results: There was no association between CYP3A polymorphisms and cord mercury concentrations. The scores for the BSID mental scale improved with increasing cord blood mercury concentrations for carriers of the most active alleles (β[95% CI]: = 2.9[1.53,4.27] for CYP3A7 rs2257401 GG + GC, 2.51[1.04,3.98] for CYP3A5 rs776746 AA + AG and 2.31[0.12,4.50] for CYP3A4 rs2740574 GG + AG). This association was near the null for CYP3A7 CC, CYP3A5 GG and CYP3A4 AA genotypes. The interaction between the CYP3A genes and total mercury was significant (p < 0.05) in European cohorts only. Conclusions: Our results suggest that the polymorphisms in CYP3A genes may modify the response to dietary MeHg exposure during early life development. ; This study was funded by Grants from Spain: Instituto de Salud Carlos III (Red INMA G03/176, CB06/02/0041, FIS-FEDER 04/1436, 09/0432, 13/1944, 13/2032, 14/00891, 14/01687, 16/1288, and Miguel Servet-FEDER CP15/0025), Fundació La marató de TV3 (090430), Conselleria de Sanitat Generalitat Valenciana, FISABIO UGP 15-230, Generalitat de Catalunya (CIRIT 1999SGR 00241); Grants from the EU: NEWGENERIS FP6-2003-Food-3-A-016320, FP7-ENV-2011 cod 282957, HEALTH.2010.2.4.5-1, and FOOD-CT-2006-016253; Grants from the US National Institutes of Health: R21-ES019954, R01-ES010219, and P30-ES01247; Grants from the Swedish Research Council FORMAS and in kind support from the government of Seychelles.
In: Ecotoxicology and environmental safety: EES ; official journal of the International Society of Ecotoxicology and Environmental safety, Band 231, S. 113194
Introduction Recycling of domestic waste and a number of employees in the recycling industry is expected to increase. This study aims to quantify current exposure levels of inhalable dust, endotoxin, and microorganisms and to identify determinants of exposure among recycling workers.
Methods This cross-sectional study included 170 full-shift measurements from 88 production workers and 14 administrative workers from 12 recycling companies in Denmark. The companies recycle domestic waste (sorting, shredding, and extracting materials from waste). We collected inhalable dust with personal samplers that were analysed for endotoxin (n = 170) and microorganisms (n = 101). Exposure levels of inhalable dust, endotoxin, and microorganisms and potential determinants of exposure were explored by mixed-effects models.
Results The production workers were 7-fold or higher exposed to inhalable dust, endotoxin, bacteria, and fungi than the administrative workers. Among production workers recycling domestic waste, the geometric mean exposure level was 0.6 mg/m3 for inhalable dust, 10.7 endotoxin unit (EU)/m3 for endotoxin, 1.6 × 104 colony forming units (CFU)/m³ of bacteria, 4.4 × 104 CFU/m³ of fungi (25 °C), and 1.0 × 103 CFU/m³ of fungi (37 °C). Workers handling paper or cardboard had higher exposure levels than workers handling other waste fractions. The temperature did not affect exposure levels, although there was a tendency toward increased exposure to bacteria and fungi with higher temperatures. For inhalable dust and endotoxin, exposure levels during outdoor work were low compared to indoor work. For bacteria and fungi, indoor ventilation decreased exposure. The work task, waste fraction, temperature, location, mechanical ventilation, and the company size explained around half of the variance of levels of inhalable dust, endotoxin, bacteria, and fungi.
Conclusion The production workers of the Danish recycling industry participating in this study had higher exposure levels of inhalable dust, endotoxin, bacteria, and fungi than the administrative workers. Exposure levels of inhalable dust and endotoxin among recycling workers in Denmark were generally below established or suggested occupational exposure limits (OEL). However, 43% to 58% of the individual measurements of bacteria and fungi were above the suggested OEL. The waste fraction was the most influential determinant for exposure, and the highest exposure levels were seen during handling paper or cardboard. Future studies should examine the relationship between exposure levels and health effects among workers recycling domestic waste.
OBJECTIVES: We investigated associations between bioaerosol exposures and work-shift changes in lung function and inflammatory markers among recycling workers. METHODS: Inhalable dust was measured with personal samplers and analyzed for endotoxin, bacteria, and fungi (incubated at 25 °C and 37 °C) levels. Lung function (FEV1, FVC) was measured before and after work-shifts and serum concentrations of inflammatory markers (CRP, SAA, CC16, IL1B, IL2, IL4, IL5, IL6, IL8, IL10, IL13, and TNF) after the shift. Associations were explored by linear mixed-effects models. RESULTS: We included 170 measurements from 88 production workers exposed to inhalable dust, endotoxin, bacteria, and fungi (25 °C and 37 °C) at geometric mean levels of 0.6 mg/m3, 10.7 EU/m3, 1.6×104 CFU/m3, 4.4×104 CFU/m3, and 103 CFU/m3, respectively, and 14 administrative workers exposed at 7-fold lower levels. No associations were observed between bioaerosol exposures and work-shift change in lung function. IL2, IL6, IL10, and TNF concentrations were positively associated with inhalable dust levels, SAA and IL6 with bacteria, CRP, SAA, IL8, and TNF with fungi (25 °C or 37 °C), with the latter being the only statistically significant finding (exp(β) 1.40, 95% confidence interval 1.01–1.96). CONCLUSIONS: This study of recycling workers exposed to bioaerosol levels generally below those of farmers and compost workers and above background levels did not indicate any acute effect on lung function. Several inflammatory markers tended to increase with exposure, suggesting a systemic effect. Future research should combine data from bioaerosol-exposed workers to uncover health risks that may form the basis for health-based occupational exposure limits.
Objective Within the scope of the Exposome Project for Health and Occupational Research on applying the exposome concept to working life health, we aimed to provide a broad overview of the status of knowledge on occupational exposures and associated health effects across multiple noncommunicable diseases (NCDs) to help inform research priorities.
Methods We conducted a narrative review of occupational risk factors that can be considered to have "consistent evidence for an association," or where there is "limited/inadequate evidence for an association" for 6 NCD groups: nonmalignant respiratory diseases; neurodegenerative diseases; cardiovascular/metabolic diseases; mental disorders; musculoskeletal diseases; and cancer. The assessment was done in expert sessions, primarily based on systematic reviews, supplemented with narrative reviews, reports, and original studies. Subsequently, knowledge gaps were identified, e.g. based on missing information on exposure–response relationships, gender differences, critical time-windows, interactions, and inadequate study quality.
Results We identified over 200 occupational exposures with consistent or limited/inadequate evidence for associations with one or more of 60+ NCDs. Various exposures were identified as possible risk factors for multiple outcomes. Examples are diesel engine exhaust and cadmium, with consistent evidence for lung cancer, but limited/inadequate evidence for other cancer sites, respiratory, neurodegenerative, and cardiovascular diseases. Other examples are physically heavy work, shift work, and decision latitude/job control. For associations with limited/inadequate evidence, new studies are needed to confirm the association. For risk factors with consistent evidence, improvements in study design, exposure assessment, and case definition could lead to a better understanding of the association and help inform health-based threshold levels.
Conclusions By providing an overview of knowledge gaps in the associations between occupational exposures and their health effects, our narrative review will help setting priorities in occupational health research. Future epidemiological studies should prioritize to include large sample sizes, assess exposures prior to disease onset, and quantify exposures. Potential sources of biases and confounding need to be identified and accounted for in both original studies and systematic reviews.
WOS: 000319871200001 ; PubMed ID: 23198723 ; Aims: Urinary 8-oxo-7,8-dihydro-2'-deoxyguanosine (8-oxodG) is a widely used biomarker of oxidative stress. However, variability between chromatographic and ELISA methods hampers interpretation of data, and this variability may increase should urine composition differ between individuals, leading to assay interference. Furthermore, optimal urine sampling conditions are not well defined. We performed inter-laboratory comparisons of 8-oxodG measurement between mass spectrometric-, electrochemical- and ELISA-based methods, using common within-technique calibrants to analyze 8-oxodG-spiked phosphate-buffered saline and urine samples. We also investigated human subject- and sample collection-related variables, as potential sources of variability. Results: Chromatographic assays showed high agreement across urines from different subjects, whereas ELISAs showed far more inter-laboratory variation and generally overestimated levels, compared to the chromatographic assays. Excretion rates in timed 'spot' samples showed strong correlations with 24 h excretion (the 'gold' standard) of urinary 8-oxodG (r(p) 0.67-0.90), although the associations were weaker for 8-oxodG adjusted for creatinine or specific gravity (SG). The within-individual excretion of 8-oxodG varied only moderately between days (CV 17% for 24 h excretion and 20% for first void, creatinine-corrected samples). Innovation: This is the first comprehensive study of both human and methodological factors influencing 8-oxodG measurement, providing key information for future studies with this important biomarker. Conclusion: ELISA variability is greater than chromatographic assay variability, and cannot determine absolute levels of 8-oxodG. Use of standardized calibrants greatly improves intra-technique agreement and, for the chromatographic assays, importantly allows integration of results for pooled analyses. If 24 h samples are not feasible, creatinine- or SG-adjusted first morning samples are recommended. ; ECNIS (Environmental Cancer Risk, Nutrition and Individual Susceptibility), a network of excellence operating within the European Union 6th Framework Program, Priority 5:"Food Quality and Safety" [FOOD-CT-2005-513943]; ECNIS2, a coordination and support action within the European Union FP7 Cooperation Theme 2 Food, Agriculture, Fisheries and Biotechnologies; CISBO; Ingeborg; Leo Dannin Foundation; National Science Council, TaiwanNational Science Council of Taiwan [NSC 97-2314-B-040-015-MY3, NSC 100-2628-B-040-001-MY4]; US NIHUnited States Department of Health & Human ServicesNational Institutes of Health (NIH) - USA [P30ES009089]; Instituto Carlos III division of the Government for Clinical Research [PI-10/00802, RD06/0045/0006]; Generalitat ValencianaGeneralitat Valenciana [ACOM/2012/238]; Swedish Council for Working Life and Social ResearchSwedish Research CouncilSwedish Research Council for Health Working Life & Welfare (Forte); TUBITAK (Technical and Scientific Research Council of Turkey)Turkiye Bilimsel ve Teknolojik Arastirma Kurumu (TUBITAK) [108Y049]; Grant Agency of the Czech RepublicGrant Agency of the Czech Republic [P503/11/0084]; Sahlgrenska University Hospital, Gothenburg; UK Medical Research Council via a People Exchange Programme Research Leader Fellowship award [G1001808/98136] ; Some of the authors of this work were partners in, and this work was partly supported by, ECNIS (Environmental Cancer Risk, Nutrition and Individual Susceptibility), a network of excellence operating within the European Union 6th Framework Program, Priority 5:"Food Quality and Safety" (Contract No. FOOD-CT-2005-513943), and also ECNIS 2 , a coordination and support action within the European Union FP7 Cooperation Theme 2 Food, Agriculture, Fisheries and Biotechnologies.; P Moller and S Loft are supported by CISBO and the Ingeborg and Leo Dannin Foundation.; M-R Chao and C-W Hu acknowledge financial support from the National Science Council, Taiwan (Grants NSC 97-2314-B-040-015-MY3 and NSC 100-2628-B-040-001-MY4).; R Santella acknowledges the contribution of Qiao Wang, and support from US NIH P30ES009089.; G Saez and C Cerda acknowledge financial support from the Instituto Carlos III division of the Government for Clinical Research (Grants PI-10/00802 and RD06/0045/0006) and Grant ACOM/2012/238 from Generalitat Valenciana.; K Broberg, C Lindh, and M Hossain acknowledge financial support from the Swedish Council for Working Life and Social Research; H Orhan and N Senduran acknowledge financial support from TUBITAK (Technical and Scientific Research Council of Turkey), grant number 108Y049.; P Rossner, Jr. and RJ Sram acknowledge support from the Grant Agency of the Czech Republic (P503/11/0084).; L Barregard acknowledges financial support from the Sahlgrenska University Hospital, Gothenburg.; MS Cooke acknowledges support from the UK Medical Research Council via a People Exchange Programme Research Leader Fellowship award (G1001808/98136).
