Changes in enzymatic antioxidant activity are frequently observed in workers occupationally exposed to lead. Few studies have investigated the influence of lead on the non-enzymatic antioxidant system. The aim of our study was to assess the influence of occupational exposure to lead on the plasma concentration of two hydrophobic forms of vitamin E: α-tocopherol and -tocopherol.
A sample of 401 healthy men, aged 19–62, participated in the study. In total, 340 of these subjects were employed at the Mine and Metallurgical Plant in southern Poland. The workers who were occupationally exposed to lead were divided into quartiles (groups of 85 subjects). The lead concentrations in the blood of the subjects in the control group and in the lead exposure quartiles correspond to the following ranges: 10–72 μg/l (control group); 82–206 μg/l (Q1); 209–308 μg/l (Q2); 308–394 μg/l (Q3) and 395–644 μg/l (Q4), respectively.
Significant differences were observed only for the plasma concentration of -tocopherol, which differed between the control group and Q1 (by 24.1%, p=0.0368), between Q1 and Q3 (by –18.8%, p=0.0115) and between Q1 and Q4 (by –25.7%, p=0.0002). Multiple linear regression analysis showed that the statistically significant, predictive properties of the -tocopherol plasma concentration were as follows: triglycerides (β=0.440)> age (β=0.131)> whole cholesterol (β=0.117)> blood lead concentration (β=–0.108). For α-tocopherol, significant prognostic properties were triglycerides and total cholesterol (β=0.485 and β=0.399, respectively).
Occupational exposure to lead is strongly correlated with the concentration of -tocopherol but not α-tocopherol.
The risk factors for sporadic (ie, non-familial) retinoblastoma remain largely unknown.
We examined the relationship between paternal occupational exposures from jobs held 10 years and 1 year prior to conception and the risk of sporadic bilateral retinoblastoma in children.
Paternal occupational data were obtained for 198 incident cases diagnosed with sporadic bilateral retinoblastoma from January 1998 to May 2006 and 245 referral-based controls from the case child's relatives and friends who were matched to 135 of the cases on birth year. Industrial hygienists independently assigned exposure scores for nine agents. Adjusted ORs and 95% CIs were computed using logistic regression models, using the full sample of cases and controls as well as subset of cases with matched controls only.
There was some indication of an elevated risk associated with paternal pesticide exposure in the 10 years prior to conception (OR=1.64; 95% CI 1.08 to 2.50) as well as in the year before conception (OR=2.12; 95% CI 1.25 to 3.61). However, results for pesticide exposure were inconsistent and varied by analysis approach. An increased risk was also observed for non-welding metal exposure during the 10 years prior to conception in the full (OR=1.35; 95% CI 0.86 to 2.12) and matched (OR=1.40; 95% CI 0.82 to 2.37) samples, but not in the year before conception. Exposure–response trends were observed for pesticides and non-welding metal exposures.
Our findings suggest a potential role of paternal occupational exposures to non-welding metals and perhaps pesticides in the aetiology of childhood retinoblastoma.
The aim of this study is to analyse if low justice at work, analysed as aggregated workplace means, increases the risk of depression.
A total of 4237 non-depressed Danish public employees within 378 different work units were enrolled in 2007. Mean levels of procedural and relational justice were computed for each work unit to obtain exposure measures that were robust to reporting bias related to depression. Two years later in 2009, 3047 (72%) participated at follow-up. Those reporting high levels of depressive, burn-out or stress symptoms were assigned to a psychiatric diagnostic interview. In the interview 58 cases of new onset depression were identified. Depression ORs by work unit level of procedural and relational justice were estimated by multivariable logistic regression accounting for established risk factors for depression.
Working in a work unit with low procedural justice (adjusted ORs of 2.50, 95% CI 1.06 to 5.88) and low relational justice (3.14, 95% CI 1.37 to 7.19) predicted onset of depression.
Our results indicate that a work environment characterised by low levels of justice is a risk factor for depression.
Excessive absorption of cobalt has been associated with cases of dilated cardiomyopathy in the past, but it is unclear whether occupationally exposed populations are at risk.
To assess the possible relationship between occupational exposure to cobalt and incipient signs of dilated cardiomyopathy.
A cross-sectional survey was conducted in a cobalt production facility in Belgium constituting one of the largest occupational populations worldwide (n=256 male workers). Exposure to cobalt was assessed by measuring urinary cobalt concentration (µg/gcreat), reflecting recent exposure, and by computing an integrated exposure index (µg/gcreatxyears), reflecting long-term exposure. The effect on the myocardium was investigated by echocardiography and electrocardiography, and dose–effect relations with cobalt exposure were traced by multiple regression analysis.
No dose–effect relationship between exposure to cobalt and parameters reflecting dilated cardiomyopathy was found in a population of workers characterised by a median recent cobalturia of 4 µg/gcreat and a median long-term cobalturia of 100 µg/gcreatxyears. A reduction in the dimensions of the left ventricular internal cavity was associated with recent exposure to cobalt.
Occupational exposure to cobalt does not appear associated with incipient signs of dilated cardiomyopathy within the gradient of exposure recorded in this population.
Trichloroethylene (TCE) and Perchloroethylene (PER) are two chlorinated solvents that are applied widely as degreasers of metal parts, and in dry cleaning and other applications. In 2012, the International Agency for Research on Cancer classified TCE as carcinogenic to humans and PER as probably carcinogenic to humans. We explored exposure–response relations for TCE and PER and non-Hodgkin's lymphoma (NHL), multiple myeloma (MM), and cancers of the kidney and liver in the Nordic Occupational Cancer cohort.
The cohort was set up by linking occupational information from censuses to national cancer registry data using personal identity codes in use in all Nordic countries. Country, time period, and job-specific exposure estimates were generated for TCE, PER and potentially confounding occupational exposures with a job-exposure matrix. A conditional logistic regression was conducted for exposure groups as well as for continuous cumulative exposure.
HRs for liver cancer, NHL and MM but not kidney cancer were slightly elevated in groups with high exposure to PER (compared to occupationally unexposed subjects). HRs for liver cancer and NHL also increased with increasing continuous exposure to PER. We did not observe evidence for an association between exposure to TCE and NHL, MM or liver and kidney cancer.
Although this study was subject to limitations related to the low prevalence of exposure to PER and TCE in the Nordic population and a limited exposure assessment strategy, we observed some evidence indicative of an excess risk of cancer of the liver and NHL in subjects exposed to PER.
Although a study among utility workers found an increased risk for acute myocardial infarction and arrhythmia-related deaths associated with occupational extremely low-frequency magnetic fields (ELF-MF) exposure, later studies largely failed to replicate these findings. This study investigated the association between occupational ELF-MF exposure and cardiovascular disease (CVD) mortality within a community-based prospective cohort study.
The Netherlands Cohort Study is a prospective cohort study among 120 852 men and women aged 55–69 years at baseline. Participants were followed-up for CVD mortality over a period of 10 years, resulting in 8200 CVD deaths. Information on occupational history and potential confounders, such as educational level, smoking and alcohol use were collected at baseline through a self-administered questionnaire. Occupational ELF-MF exposure was assigned using a job-exposure matrix. Associations with CVD mortality were analysed using Cox regression.
Ever low or high exposure to ELF-MF showed no association with total CVD mortality (HR of 1.02, 95% CI 0.99 to 1.06), nor with any cause-specific subtypes of CVD mortality. Other ELF-MF exposure metrics showed no increased risks either.
In this study, we found no indication of an association between occupational ELF-MF exposure and risk of CVD mortality.
To determine if deployment to recent military operations or other health, demographic, or military-related characteristics were associated with employment after military service.
Former US active duty military service members participating in the Millennium Cohort Study, a population-based sample of US military personnel that began in July of 2001, were prospectively followed from the time of baseline health reporting to self-reported employment status after military separation.
Of the 9099 separated personnel meeting inclusion criteria, 17% reported unemployment after military service. In multivariable modelling, prior deployment experiences, with or without reported combat, and post-traumatic stress disorder (PTSD) were not significantly associated with employment status postservice. Among those who routinely retired from service with a pension, positive screens for depression (OR, 1.67; 95% CI, 1.05 to 2.63) and panic/anxiety (OR, 1.63; 95% CI, 1.10 to 2.43) were significantly associated with subsequent unemployment. Poor physical health, female sex, black race, lower education and disabling illnesses/injuries were also predictive of postservice unemployment.
After stratifying for reason for military separation, mental disorders like depression or panic/anxiety and poor physical health may have greater impact than prior deployment experiences or PTSD on the ability to find or maintain employment postservice. These findings may guide support for veterans most in need of job placement services after military service.
Recent investigations have associated airborne particulate matter (PM) with increased coagulation and thrombosis, but underlying biological mechanisms are still incompletely characterised. DNA methylation is an environmentally sensitive mechanism of gene regulation that could potentially contribute to PM-induced hypercoagulability.
We aimed to test whether altered methylation mediates environmental effects on coagulation.
We investigated 63 steel workers exposed to a wide range of PM levels, as a work-related condition with well-characterised prothrombotic exposure. We measured personal PM10 (PM≤10 µm in aerodynamic diameter), PM1 (≤1 µm) and air metal components. We determined leukocyte DNA methylation of NOS3 (nitric-oxide-synthase-3) and EDN1 (endothelin-1) through bisulfite-pyrosequencing and we measured ETP as a global coagulation-activation test after standardised triggers.
ETP increased in association with PM10 (β=20.0, 95% CI 3.0 to 37.0), PM1 (β=80.8 95% CI 14.9 to 146.7) and zinc (β=51.3, 95% CI 0.01 to 111.1) exposures. NOS3 methylation was negatively associated with PM10 (β=–0.2, 95% CI –0.4 to –0.03), PM1 (β=–0.8, 95% CI –1.4 to –0.1), zinc (β=–0.9, 95% CI –1.4 to –0.3) and iron (β=–0.7, 95% CI –1.4 to –0.01) exposures. Zinc exposure was negatively associated with EDN1 (β=–0.3, 95% CI –0.8 to –0.1) methylation. Lower NOS3 (β=–42.3; p<0.001) and EDN1 (β=–14.5; p=0.05) were associated with higher ETP. Statistical mediation analysis formally confirmed NOS3 and EDN1 hypomethylation as intermediate mechanisms for PM-related coagulation effects.
Our study showed for the first time, that gene hypomethylation contributes to environmentally induced hypercoagulability.
Ambient fine-particle particulate matter (PM2.5) exposure is associated with the decline in pulmonary function, prevalence of coronary heart disease and incidence of myocardial infarction. The study is to observe the effects of ambient PM2.5 on the cardiovascular system and to explore the potential inflammatory and immune mechanisms.
The subjects included 110 traffic policemen in Shanghai, China, who were aged 25–55 years. Two-times continuous 24 h individual-level PM2.5 measurements were performed in winter and summer, respectively. The inflammatory marker (high-sensitivity C-reactive protein, hs-CRP), immune parameters (IgA, IgG, IgM and IgE) and lymphocyte profiles (CD4 T cells, CD8 T cells, CD4/CD8 T cells) were measured in blood. The associations between individual-level PM2.5 and inflammatory marker and immune parameters were analysed by multiple linear regression.
The average concentration of 24 h personal PM2.5 for participants was 116.98 μg/m3 and 86.48 μg/m3 in winter and summer, respectively. In the main analysis, PM2.5 exposure is associated with the increases in hs-CRP of 1.1%, IgG of 6.7%, IgM of 11.2% and IgE of 3.3% in participants, and decreases in IgA of 4.7% and CD8 of 0.7%, whereas we found no statistical association in CD4 T cells and CD4/CD8 T cells. In the adjusted model, the results showed that the increase of PM2.5 was associated with the changes of inflammatory markers and immune markers both in winter and summer.
Traffic policeman have been a high-risk group suffering inflammatory response or immune injury because of the high exposure to PM2.5. These findings provided new insight into the mechanisms linking ambient PM2.5 and inflammatory and immune response.
Outbreaks of Saharan dust have been shown to exacerbate the effect of particulate matter (PM) on mortality. Their role on PM–morbidity association is less clear. This study aims to evaluate the effect of Saharan dust on the PM–hospitalisations association in Rome, Italy.
We studied residents hospitalised in Rome between 2001 and 2004 and performed a time-series analysis to explore the effects of PM2.5, PM2.5–10 and PM10 on cardiac, cerebrovascular and respiratory emergency hospitalisations, respectively. Saharan dust days were identified by combining Light Detection and Ranging observations and analyses from operational models. We tested a dust–PM interaction to evaluate the hypothesis that the PM effect on hospitalisations would be enhanced on dust days.
We studied 77 354, 26 557 and 31 620 hospitalisations for cardiac, cerebrovascular and respiratory diseases, respectively, providing effect estimates per IQR. PM2.5–10 was associated with cardiac diseases (3.93%; 95% CI 1.58 to 6.34). PM10 was associated with cardiac (3.37%; 95% CI 1.11 to 5.68), cerebrovascular (2.64%; 95% CI 0.06 to 5.29) and respiratory diseases (3.59%: 95% CI 0.18 to 7.12). No effect of PM2.5 was detected. Saharan dust modified the effect of the PM2.5–10 on respiratory hospitalisations, higher during dust days compared with dust-free days (14.63% vs –0.32%; p value of interaction=0.006). Saharan dust also increased the effect of PM10 on cerebrovascular diseases (5.04% vs 0.90%, p value of interaction=0.143).
A clear enhanced effect of PM2.5–10 on respiratory diseases and of PM10 on cerebrovascular diseases emerged during Saharan dust outbreaks.
Patient 1 had been applying tape to pipes in non-ventilated, underground apartments for 5 days before he developed a slow reaction time, headache, nausea and vomiting. He worked 10 h per day with a 10-min break in both the morning and the afternoon. The adhesive tape he used produced a strong smell, and he did not wear any personal protective equipment. Patient 2 had been painting internal walls for 6 days before he developed headache, nausea, vomiting, diplopia and intermittent drowsiness. He worked in confined spaces for up to 8 h at a time without any protective equipment. He complained of irritated...]]>