Anapafseos 5 . Agios Nikolaos
Crete.Greece.72100
2841026182
CONSTANCES is a general-purpose cohort with a focus on occupational and environmental factors.
Cohort participantsCONSTANCES was designed as a randomly selected sample of French adults aged 18–69 years at inception; 200 000 participants will be included.
Data collection phasesAt enrolment, the participants are invited to complete questionnaires and to attend a health screening centre (HSC) for a health examination. A biobank will be set up. The follow-up includes an yearly self-administered questionnaire, a periodic visit to an HSC and linkage to social and national health administrative databases.
Main types of data collectedData collected for participants include social and demographic characteristics, socioeconomic status, life events and behaviours. Regarding occupational and environmental factors, a wealth of data on organisational, chemical, biological, biomechanical and psychosocial lifelong exposure, as well as residential characteristics, are collected at enrolment and during follow-up. The health data cover a wide spectrum: self-reported health scales, reported prevalent and incident diseases, long-term chronic diseases and hospitalisations, sick-leaves, handicaps, limitations, disabilities and injuries, healthcare usage and services provided, and causes of death.
Control of selection effectsTo take into account non-participation and attrition, a random cohort of non-participants was set up and will be followed through the same national databases as participants.
Data accessInclusions begun at the end of 2012 and more than 110 000 participants were already included by September 2016. Several projects on occupational and environmental risks already applied to a public call for nested research projects.
The association between ambient heat and neural tube defects has received limited attention, despite imminent climate warming this century. We sought to determine the relationship between elevated outdoor temperatures during neurogenesis and risk of neural tube defects.
MethodsWe carried out a retrospective cohort study of 887 710 fetuses between 3 and 4 weeks postconception from the months of April through September for 1988–2012 in Quebec, Canada. The exposure was maximum daily temperature and the outcome presence of neural tube defects at delivery. We estimated prevalence ratios (PR) and 95% CIs for the association between maximum temperature and neural tube defects in log-binomial regression models adjusted for maternal characteristics.
ResultsRelative to 20°C, exposure to temperatures of 30°C was associated with risk of neural tube defects on day 5 (PR 1.56, 95% CI 1.04 to 2.35) and day 6 (PR 1.49, 95% CI 1.00 to 2.21) of the 4th week postconception, during the time of neural tube closure. The trend was apparent for spina bifida and anencephalus/encephalocoele, the main subtypes of neural tube defects. Temperature during the 3rd week postconception was not associated with neural tube defects.
ConclusionsElevated ambient temperatures may be weakly associated with risk of neural tube defects during tube closure.
‘Exposure–response relationships between movements and postures of the wrist and carpal tunnel syndrome among male and female house painters: a retrospective cohort study’, by Heilskov-Hansen et al,1 is a welcome addition to the carpal tunnel syndrome (CTS) literature. The authors explored relations between incidence of CTS and wrist movements, wrist postures and sex. They discovered a higher incidence related to velocity of wrist movements and frequency of repetitions, but no cumulative effect. Furthermore, the paper showed an absolute higher CTS incidence in women than in men.
Prior study shows that CTS incidence is higher in working populations, but the link to intense and repetitive manual tasks is unclear.2 Heilskov-Hansen et al shed light on this topic, revealing the possible role of task-specific hand use in the increased incidence of CTS.
The most remarkable finding of the current study is the observed difference between women and men. The authors...
We thank Coraci and colleagues1 for their comments on our study.2
We fully agree on the importance of using objective quantitative outcome measures, since this is essential for evaluating the correlation between carpal tunnel syndrome (CTS) and different work exposures or other individual characteristics. In time, this can lead to prevention, diagnosis, treatments and rehabilitation, specific to the individual worker.
When deciding on an objective measuring method, one needs to consider the feasibility when applied on a population of a sufficient size. We acknowledge Coraci and colleagues suggestion of using ultrasonography as an objective measure. However, from what exists in the current literature we are not convinced that value adding correlations can be made between neurophysiological measured median nerve function and work tasks. In future research, attempts should be made to apply the same metrics when examining CTS, thus allowing the results to be aggregated in a job...
The aim of this study is to evaluate whether exposure to low concentrations of cadmium (Cd) can have effects on the thyroid hormone level of outdoor workers exposed to urban pollutants.
Methods:The study was conducted on a final sample of 277 individuals (184 males and 93 females). The environmental monitoring of Cd was evaluated through the use of portable dosimeters, while the biological monitoring was achieved through the assessment of urinary Cd and thyroid hormones. The total sample was divided according to sex and task. The Pearson’s correlation coefficient among the variables was calculated after subdivision on the basis of sex and task. The multiple linear regression was performed to take into account the major confounding factors.
Results:Statistical tests showed a negative correlation between urinary Cd levels and free triiodothyronine and free thyroxine and a positive correlation between urinary Cd and thyroid-stimulating hormone levels.
Conclusions:Our early results seem to point out that occupational exposure to low concentrations of Cd present in urban air affects the thyroid hormone levels in exposed workers.
Flumetralin, a synthetic plant growth regulator with herbicidal activity belonging to the 2,6-dinitroaniline class of chemicals, has been evaluated for its ability to induce genotoxicity in human peripheral blood lymphocytes (PBLs). The potential genotoxic and cytotoxic effects of flumetralin were investigated in vitro by chromosome aberration (CA) and cytokinesis-block micronucleus assays. Human PBLs were treated with 125, 250, 500, and 1000 µg/mL flumetralin for 24 and 48 h. Flumetralin statistically significantly increased the frequency of structural CAs at the three highest concentrations (250, 500, and 1000 µg/mL) for both treatment periods (24 and 48 h) when compared with both the negative and solvent controls. In addition, micronucleus formation was significantly induced at higher concentrations (250, 500, and 1000 µg/mL) for 24 h and at 125 and 500 µg/mL of flumetralin for the 48-h treatment period compared with the controls. Because of the excessive cytostatic effects of flumetralin, binuclear cells could not be detected sufficiently at the highest two concentrations (500 and 1000 µg/mL) for the 48-h treatment period. Furthermore, flumetralin significantly decreased the mitotic index and nuclear division index for all concentrations and treatment times compared with the control groups. The present results indicate that flumetralin was clastogenic and cytotoxic/cytostatic to human PBLs. This study presents the first report of the genotoxic and cytotoxic properties of flumetralin.
Vinyl chloride monomer (VCM) is widely used in the production of polyvinyl chloride (PVC) plastics. VCM is recognized as a confirmed human and animal carcinogenic compound. Recent studies have reported poor health of plastic workers, even having exposure at concentrations below the permissible limit to VCM. There has not been any study regarding exposed workers to VCM in Iran. Similarly, no information exists as to the biological monitoring of such workers. The main purpose of this study was to conduct a thorough occupational and biological monitoring of Iranian plastic workers exposed to VCM.
A total of 100 workers from two plastic manufacturing plants (A and B) in Tehran along with 25 unexposed workers as controls were studied. The personal monitoring of all nonsmoking workers exposed to VCM at two plastic manufacturing plants (A and B) was performed in the morning shift (8 a.m. to 4 p.m.) according to the National Institute For Occupational Safety And Health method no. 1007.
Biological monitoring of workers was carried out through collection of exhaled breath of all exposed and control workers in Tedlar bags and with a subsequent analysis using gas chromatography–flame ionization detector.
Not only the mean occupational exposure of workers to VCM at plant A was higher than the respective threshold limit value but also the statistical significance was higher than workers at plant B. Similarly, VCM concentration in exhaled breath of workers at plant A was also statistically significantly higher than at plant B. Correlation of occupational exposure of all workers to vinyl chloride with its concentration in exhaled breath was statistically significant.
This is the first study on biological monitoring for exposed plastic workers to VCM using exhaled breath. On the basis of the results in this study, a novel method of biological monitoring of plastic workers was proposed.
Exposure to arsenic and mercury is known to cause respiratory problems in both humans and animals. In this study, we elicit and compare maximum contraction caused by As(III) and Hg(II) when the pollutants are fully equilibrated with contractile machinery in resting mode. Hypercontraction of 27% and 69% was obtained following exposure of tracheal rings to 25 µM As(III) and 6 nM Hg(II) for 40 min, respectively. Co-incubation of tracheal rings with pollutants and verapamil, sodium nitroprusside or apocynin indicates that major contributors to As(III) and Hg(II) caused hypercontraction are reactive oxygen species (ROS) elevation and nitric oxide (NO) depletion. Changes in calcium influx have minor contribution in As(III) and Hg(II) caused increased contraction of tracheal tissues. Eugenol and carvone caused relaxation of 38% and 45% in pollutant unexposed rings, 56% and 49% in As(III)-exposed tracheal rings, and 54% and 47% in Hg(II)-exposed tracheal rings. Pathway delineation studies indicate that the major effect of eugenol originates from quenching of ROS whereas that of carvone originates from the blockage of extracellular calcium influx. Both molecules also show a minor stimulatory effect on NO generation. In line with their suggested mode of relaxation, eugenol is found to better ameliorate both As(III)- and Hg(II)-caused hypercontraction. Carvone, though a better relaxant than eugenol, comes out as poor ameliorator of both As(III)- and Hg(II)-caused hypercontraction, as the pathway on which it acts is not elevated following exposure to these pollutants.
Previous cross-sectional studies have shown that exposure to cleaning chemicals among health-care workers (HCWs) is associated with respiratory disorders and ventilatory function changes. This study aimed to further explore this association using a longitudinal approach. A prospective 2-year follow-up study was carried out at a tertiary care hospital in Saudi Arabia from June 2012 to June 2014 among 56 nurses who were responsible for disinfection and sterilization of medical instruments and equipment. The workplaces of the participants were assessed for engineering, environmental, and safety control measures. Self-administered questionnaires were distributed to all participants to assess their exposure to cleaning chemicals and their medical history. Spirometric parameters were measured for all nurses in 2012 (baseline) and again in 2014 (follow-up). The prevalence of work-related respiratory symptoms did not increase significantly over this time. Among all the spirometric parameters, only forced expiratory volume in 1 second (FEV1)/forced vital capacity (FVC) ratio decreased significantly, and only 10.7% of participants who were exposed to cleaning chemicals for more than 10 years had FEV1 and FVC less than their longitudinal normal limits at the end of the study. Smoking and gender were associated with statistically significant decreases in some of the spirometric parameters. Our 2-year follow-up study did not demonstrate significant association between exposure to cleaning chemicals among HCWs and changes in the prevalence of work-related respiratory symptoms, but indicated early effects on ventilatory function among them. The study highlights the importance of periodic spirometry, proper work practices, and effective control measures to protect HCWs against potentially harmful workplace chemicals for disinfection and sterilization.
In this study, we aimed to investigate the extent of genotoxic risk and the association between null GSTM1/GSTT1 and GSTP1 Ile105Val variants and cellular DNA damage, as measured by micronucleus (MN) assay in a group of agricultural workers from Denizli, Turkey. Peripheral blood samples were collected from 116 subjects, including 58 workers who were occupationally exposed to pesticides and 58 healthy unexposed controls. The MN frequencies of each individual were assessed by cytokinesis-blocked micronuclei assays on lymphocytes. Genotypes for different GST variants were determined using polymerase chain reaction-based methods. A significant 3.4-fold increase in MN frequency was observed in workers compared with the controls (p < 0.001). Among the GST genotypes, only the GSTM1 null genotype was found to be significantly associated with an increased MN frequency in workers (p = 0.01). Individuals with a concomitant null GSTM1/GSTT1 genotype demonstrated a significant (p = 0.01) increase in MN frequency compared with those with functional isozymes in the exposed worker group. The association of the GSTM1 null genotype with higher MN frequency suggests that it may be a modifier of genotoxic risk in individuals exposed to pesticides and may thus be a candidate susceptibility biomarker for human biomonitoring studies.
Pulmonary complications of exposure to sulfur mustard (SM) gas range from no effect or mild symptoms to severe bronchial stenosis. In the present study, the protective effect of vitamin E on the lung inflammation of SM-exposed guinea pigs was examined. Guinea pigs (n = 5 for each group) were exposed to ethanol (control group), 40 mg/m3 inhaled SM (SME group), SME treated with vitamin E (SME + E), SME treated with dexamethasone (SME + D), and SME treated with both treatments (SME + E + D). Pathological evaluation of the lung was done 14 days postexposure. The epithelial desquamation of trachea and other pathologic changes in the lung of the SME group were significantly higher than those in the control group. Furthermore, the pathological changes of trachea and lung in the SME + E and SME + E + D groups were significantly improved compared with those of SME group. In addition, the pathological changes of trachea and lung of SME + E and SME + E + D animals were significantly less than those of SME + D group.
Ethylbenzene is an important industrial chemical, but its potential toxicity is a recent concern. Our previous study investigated the renal toxicity of ethylbenzene in vivo. Rat renal epithelial cells (NRK-52E cells) were incubated with 0, 30, 60, and 90 µmol/L of ethylbenzene for 24 h in vitro to investigate ethylbenzene-induced oxidative stress, apoptosis, and the expression of heme oxygenase 1 (HO-1) and nuclear factor (erythroid 2)-related factor 2 (Nrf2). The cell survival rate in the ethylbenzene-treated groups was significantly lower than the control group. Ethylbenzene significantly increased intracellular reactive oxygen species and apoptosis. Malondialdehyde levels were significantly elevated compared with the control group, while glutathione levels and glutathione peroxidase activities were decreased in ethylbenzene-treated groups. The activities of catalase and superoxide dismutase were also markedly reduced. A significant dose-dependent increase in HO-1 and Nrf2 messenger RNA expression levels was observed in ethylbenzene-treated groups compared with the control group. Similarly, ethylbenzene treatment enhanced protein expression of HO-1 and Nrf2 in a dose-dependent manner. Our results indicated that ethylbenzene induced oxidative stress, apoptosis, and upregulation of HO-1 and Nrf2 in NRK-52E cells, which contributes to ethylbenzene-induced renal toxicity.
Zinc oxide nanoparticles (ZnONP) are manufactured on a large scale and can be found in a variety of consumer products, such as sunscreens, lotions, paints and food additives. Few studies have been carried out on its genotoxic potential and related mechanisms in whole organisms. In the present study, the in vivo genotoxic activity of ZnONP and its bulk form was assayed using the wing-spot test and comet assay in Drosophila melanogaster. Additionally, a lipid peroxidation analysis using the thiobarbituric acid assay was also performed. Results obtained with the wing-spot test showed a lack of genotoxic activity of both ZnO forms. However, when both particle sizes were tested in the comet assay using larvae haemocytes, a significant increase in DNA damage was observed for ZnONP treatments but only at the higher dose applied. In addition, the lipid peroxidation assay showed significant malondialdehyde (MDA) induction for both ZnO forms, but the induction of MDA for ZnONP was higher for the ZnO bulk, suggesting that the observed DNA strand breaks could be induced by mediated oxidative stress. The overall data suggest that the potential genotoxicity of ZnONP in Drosophila can be considered weak according to the lack of mutagenic and recombinogenic effects and the induction of primary DNA damage only at high toxic doses of ZnONP. This study is the first assessing the genotoxic and oxidative stress potential of nano and bulk ZnO particles in Drosophila.
The negative health effects caused by lead (Pb) exposure are widely recognized; however, the molecular mechanisms remain unknown. The aim of this study was to assess the effect of occupational Pb exposure on telomere length and to investigate the potential mechanisms leading to telomere shortening. A cohort of 334 male Pb smelters (exposed group) and 60 age-adjusted males unexposed to Pb (control group) were examined. Assessments of relative telomere length (rTL) and telomerase reverse transcriptase (TERT) gene expression were performed using quantitative real-time polymerase chain reactions. Assessments of whole blood Pb (B-Pb) and whole blood cadmium (B-Cd) concentrations and serum selenium concentration (S-Se) were performed using graphite furnace atomic absorption spectrometry. We analyzed total oxidation status (TOS), lipid hydroperoxides (LHPs), malonylodialdehyde levels in serum (MDA) and in erythrocyte hemolysates (MDA-hgb), and 8-hydroxy-deoxy-guanosine (8-OHdG). The Pb-exposed group had higher B-Pb values and shorter rTL than the control group. The arithmetic mean values calculated for B-Pb were 33 µg/dL versus 2.2 µg/dL (p < 0.0001), and the rTL values were 0.928 and 1.126 relative units (p = 0.001), respectively, for the Pb-exposed and control groups. The rTL was found to gradually shorten in response to the increasing levels of Pb exposure. The Pb-exposed group also demonstrated a higher level of oxidative stress than the control group, which was indicated by increased TOS and MDA-hgb values. rTL was negatively associated with parameters that indicated increased oxidative stress, including TOS (Spearman’s rank coefficient (rS) = –0.16; p < 0.01) and MDA-hgb (rS = –0.17; p < 0.001). No correlations were found between rTL and B-Cd and S-Se or smoking and MDA and LHP levels. Univariate analysis indicated that B-Pb was associated with decreased rTL (β =–0.0041; p = 0.0063) and that the association between B-Pb and rTL remained significant, even when adjusting for age (β = –0.0041; p = 0.0065) and in multivariable-adjusted model (β = –0.0042; p = 0.0063). In conclusion, occupational Pb exposure resulted in decreased rTL and may represent a mechanism that contributes to Pb-related diseases.
In the present studies, the in vitro and in vivo efficacies of a novel cyanide countermeasure, dimethyl trisulfide (DMTS), were evaluated. DMTS is a sulfur-based molecule found in garlic, onion, broccoli, and similar plants. DMTS was studied for effectiveness as a sulfur donor-type cyanide countermeasure. The sulfur donor reactivity of DMTS was determined by measuring the rate of the formation of the cyanide metabolite thiocyanate. In experiments carried out in vitro in the presence of the sulfurtransferase rhodanese (Rh) and at the experimental pH of 7.4, DMTS was observed to convert cyanide to thiocyanate with greater than 40 times higher efficacy than does thiosulfate, the sulfur donor component of the US Food and Drug Administration-approved cyanide countermeasure Nithiodote®. In the absence of Rh, DMTS was observed to be almost 80 times more efficient than sodium thiosulfate in vitro. The fact that DMTS converts cyanide to thiocyanate more efficiently than does thiosulfate both with and without Rh makes it a promising sulfur donor-type cyanide antidote (scavenger) with reduced enzyme dependence in vitro. The therapeutic cyanide antidotal efficacies for DMTS versus sodium thiosulfate were measured following intramuscular administration in a mouse model and expressed as antidotal potency ratios (APR = LD50 of cyanide with antidote/LD50 of cyanide without antidote). A dose of 100 mg/kg sodium thiosulfate given intramuscularly showed only slight therapeutic protection (APR = 1.1), whereas the antidotal protection from DMTS given intramuscularly at the same dose was substantial (APR = 3.3). Based on these data, DMTS will be studied further as a promising next-generation countermeasure for cyanide intoxication.
Lack of physical activity (PA) has been hypothesised as an underlying mechanism in the adverse health effects of shift work. Therefore, our aim was to compare non-occupational PA levels between shift workers and non-shift workers. Furthermore, exposure–response relationships for frequency of night shifts and years of shift work regarding non-occupational PA levels were studied.
MethodsData of 5980 non-shift workers and 532 shift workers from the European Prospective Investigation into Cancer and Nutrition-Netherlands (EPIC-NL) were used in these cross-sectional analyses. Time spent (hours/week) in different PA types (walking/cycling/exercise/chores) and intensities (moderate/vigorous) were calculated based on self-reported PA. Furthermore, sports were operationalised as: playing sports (no/yes), individual versus non-individual sports, and non-vigorous-intensity versus vigorous-intensity sports. PA levels were compared between shift workers and non-shift workers using Generalized Estimating Equations and logistic regression.
ResultsShift workers reported spending more time walking than non-shift workers (B=2.3 (95% CI 1.2 to 3.4)), but shift work was not associated with other PA types and any of the sports activities. Shift workers who worked 1–4 night shifts/month (B=2.4 (95% CI 0.6 to 4.3)) and ≥5 night shifts/month (B=3.7 (95% CI 1.8 to 5.6)) spent more time walking than non-shift workers. No exposure–response relationships were found between years of shift work and PA levels.
ConclusionsShift workers spent more time walking than non-shift workers, but we observed no differences in other non-occupational PA levels. To better understand if and how PA plays a role in the negative health consequences of shift work, our findings need to be confirmed in future studies.
In a previous editorial in this journal1 we have argued that there are likely to be important occupational causes of neurodegenerative diseases, including amyotrophic lateral sclerosis (ALS) (also commonly known as motor neuron disease) which have not yet been discovered or established.
However, for most neurodegenerative diseases, including ALS, the epidemiology has not been ‘done’, and there have been relatively few high-quality studies, in contrast to the situation with other non-communicable diseases (NCDs) such as cancer and respiratory disease.
Nevertheless, a number of occupational exposures are suspected of contributing to the risk of ALS,2 including agricultural chemicals, metals, welding fume, electric shocks and extremely low-frequency electromagnetic fields (ELF-EMFs)3 and organic solvents (eg, formaldehyde), although the evidence to date is inconsistent. Recently, a cluster of motor neurone disease (MND) cases has been linked to exposure to the fumigant methyl bromide.4 Other putative risk factors include...
The vertebral cross-sectional area (CSA) is a major determinant of vertebral strength. Since leisure-time physical activity (LTPA) is known to affect vertebral CSA, we hypothesised that engagement in physical activity at work might have similar effects on vertebral size. We aimed to examine the association between various adulthood occupational physical activities (OPA) and vertebral CSA, and to evaluate the association between OPA intensity and vertebral CSA.
MethodsWe used the prospective population-based Northern Finland Birth Cohort 1966. Our sample consisted of 712 participants with a mean age of 46.8 years. We assessed their engagement in various individual physical work activities at the ages of 31 and 46, and created overall OPA categories (high, moderate and low intensity), which we used in the analyses to study their association with vertebral CSA in middle age. Linear regression was used as the statistical method with adjustments for LTPA, vertebral height, body mass index and smoking.
ResultsA statistically significant association was found between occupational sitting and smaller vertebral CSA in men, but only at the age of 31 (49.2 mm2 smaller among those who sit often vs rarely (95% CI –96.0 to –2.4)). No significant differences were detected between OPA categories and vertebral CSA (p>0.05). Thus, we found no consistent association between OPA and vertebral size among either sex.
ConclusionsOPA seems to have very little effect on vertebral size. Our results suggest that the effect of LTPA on vertebral size is different to that of OPA.
Underemployment occurs when workers are available for more hours of work than offered. It is a serious problem in many Organisation for Economic Co-operation and Development (OECD) countries, and particularly in Australia, where it affects about 8% of the employed population. This paper seeks to answer the question: does an increase in underemployment have an influence on mental health?
MethodsThe current paper uses data from an Australian cohort of working people (2001–2013) to investigate both within-person and between-person differences in mental health associated with being underemployed compared with being fully employed. The main exposure was underemployment (not underemployed, underemployed 1–5, 6–10, 11–20 and over 21 hours), and the outcome was the five-item Mental Health Inventory.
ResultsResults suggest that stepwise declines in mental health are associated with an increasing number of hours underemployed. Results were stronger in the random-effects (11–20 hours =–1.53, 95% CI –2.03 to –1.03, p<0.001; 21 hours and over –2.24, 95% CI –3.06 to –1.43, p<0.001) than fixed-effects models (11–20 hours =–1.11, 95% CI –1.63 to –0.58, p<0.001; 21 hours and over –1.19, 95% CI –2.06 to –0.32, p=0.008). This likely reflects the fact that certain workers were more likely to suffer the negative effects of underemployment than others (eg, women, younger workers, workers in lower-skilled jobs and who were casually employed).
ConclusionsWe suggest underemployment to be a target of future workplace prevention strategies.