Long working hours may be associated with cardiovascular disease (CVD). The objective was to investigate cross-sectional associations of work hours with carotid intima media thickness (CIMT) and ankle brachial index (ABI).
Participants were 1,694 women and 1,868 men from the Multi-Ethnic Study of Atherosclerosis. CIMT and ABI were measured using standard protocols. Information on work hours was obtained from questionnaires. Mean values of CIMT and ABI were examined across five categories of hours worked per week (≤20, 21-39, 40, 41-50, >50) using ANOVA/ANCOVA. P-values for trend were obtained from linear regression models.
Mean age of participants was 56.9±8.4 years; 52.4% were men. Distinct patterns of association between work hours and the subclinical CVD biomarkers were found for women and men, although this heterogeneity by gender was not statistically significant. Among women only, work hours were positively associated with common (but not internal) CIMT (p=0.073) after full risk factor adjustment. Compared to women working 40 hours, those working >50 hours were more likely to have an ABI <1 (vs. 1-1.4) (OR=1.85, 95% CI=1.01-3.38). In men, work hours and ABI were inversely associated (p=0.046). There was some evidence that the association between work hours and ABI was modified by occupational category (interaction p=0.061). Among persons classified as Management/Professionals, longer work hours was associated with lower ABI (p=0.015). No significant associations were observed among other occupational groups.
Working longer hours may be associated with subclinical CVD. These associations should be investigated using longitudinal studies.
Atherosclerosis; carotid artery stenosis; ankle-brachial index; work
Whereas accumulating evidence indicates close associations between rhinitis and asthma, little is known about the relationships between occupational rhinitis (OR) and occupational asthma (OA). This study analyses the prevalence of OR associated with OA, globally and according to the various causal agents, and investigates the temporal relationships between these two conditions.
Data on incident cases of OA (2008–2010) were collected through the French national occupational disease surveillance and prevention network, using a standardized form including information on occupation, causal agents, presence of OR, and respective dates of occurrence of rhinitis and asthma.
Among the 596 reported OA cases with latency period, 555 could be attributed to identified agents: high molecular weight (HMW) agents (n=174); low molecular weight (LMW) agents (n=381). Overall, OR was associated with OA in 324 (58.4%) cases. The frequency of association was significantly higher for HMW agents than for LMW agents (72.2% vs 51.5%, p<0.001). OR occurred before OA significantly more frequently for HMW agents than for LMW agents (p<0.01).
These results show that OR is frequently associated with OA, especially when HMW agents are involved. They are consistent with the hypothesis that OR, in conjunction with OA, is more likely to be caused by sensitizers that cause disease via IgE-mediated mechanisms and suggest that symptoms of OR should be taken into account in the medical surveillance of workers exposed to HMW agents.
Adult; Air Pollutants, Occupational; adverse effects; chemistry; Asthma, Occupational; epidemiology; etiology; Female; France; epidemiology; Humans; Incidence; Male; Middle Aged; Molecular Weight; Occupational Diseases; epidemiology; etiology; Occupations; statistics & numerical data; Odds Ratio; Prevalence; Rhinitis; epidemiology; etiology; occupational asthma; occupational rhinitis; high molecular weight; low molecular weight
Current understanding of the dose-response relationship between occupational noise and hearing loss is based on cross-sectional studies prior to the widespread use hearing protection and with limited data regarding noise exposures below 85dBA. We report on the hearing loss experience of a unique cohort of industrial workers with daily monitoring of noise inside of hearing protection devices.
At an industrial facility, workers exhibiting accelerated hearing loss were enrolled in a mandatory program to monitor daily noise exposures inside of hearing protection. We compared these noise measurements (as time-weighted LAVG) to interval rates of high frequency hearing loss over a six year period using a mixed effects model, adjusting for potential confounders.
Workers’ high frequency hearing levels at study inception averaged more than 40 dB hearing threshold level (HTL). Most noise exposures were less than 85dBA (mean LAVG 76 dBA, interquartile range 74 to 80 dBA). We found no statistical relationship between LAvg and high frequency hearing loss (p = 0.53). Using a metric for monthly maximum noise exposure did not improve model fit.
At-ear noise exposures below 85dBA did not show an association with risk of high frequency hearing loss among workers with substantial past noise exposure and hearing loss at baseline. Therefore, effective noise control to below 85dBA may lead to significant reduction in occupational hearing loss risk in such individuals. Further research is needed on the dose response relationship of noise and hearing loss in individuals with normal hearing and little prior noise exposure.
Hearing loss; Noise induced; Dose response
Telomere length has been proposed as a biomarker of cell senescence, which is associated with a wide array of adverse health outcomes. While work is a major determinant of health, few studies have investigated the association of telomere length with various dimensions of occupation. Accelerated cellular aging could be a common pathway linking occupational exposure to several health outcomes.
Leukocyte telomere length was assessed using quantitative polymerase chain reaction (Q-PCR) in a community-based sample of 981 individuals (age: 45–84 years old). Questionnaires were used to collect information on current employment status, current or main occupation before retirement, and job strain. The O*NET (Occupational Resource Network) database was linked to the questionnaire data to create 5 exposure measures: physical activity on the job, physical hazard exposure, interpersonal stressors, job control, and job demands. Linear regression was used to estimate associations of occupational characteristics with telomere lengths after adjustment for age, sex, race, socioeconomic position, and several behavioral risk factors.
There were no mean differences in telomere lengths across current employment status, occupational category, job strain categories or levels of most O*NET exposure measures. There was also no evidence that being in lower status occupational categories or being exposed to higher levels of adverse physical or psychosocial exposures accelerated the association between age and telomere shortening.
Cellular aging as reflected by shorter telomeres does not appear to be an important pathway linking occupation to various health outcomes.
The risk factors for sporadic (i.e. non-familial) retinoblastoma remain largely unknown. However, some studies have suggested a role for paternal work activities, primarily in farming and the metalworking industry, in the development of childhood retinoblastoma.
We examined the relationship between paternal occupational exposures from jobs held 10 years and one 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, including estimates of probability, intensity, and frequency as well as an overall summary exposure score. Adjusted odds ratios (ORs) and 95% confidence intervals (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: 1.08-2.50) as well as in the year before conception (OR= 2.12; 95% CI: 1.25-3.61). 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: 0.86-2.12) and matched (OR= 1.40; 95% CI: 0.82-2.37) samples, but not in the year before conception. Exposure-response trends were observed for pesticides in the full sample (p for trend < 0.0001), and consistently across both samples for non-welding metal exposures.
Our findings suggest a potential role of paternal occupational exposures to non-welding metals and perhaps pesticides in the etiology of childhood retinoblastoma.
germline mutation; retinoblastoma; child; occupational exposure; case-control studies
Evaluating occupational exposures in population-based case-control studies often requires exposure assessors to review each study participants' reported occupational information job-by-job to derive exposure estimates. Although such assessments likely have underlying decision rules, they usually lack transparency, are time-consuming and have uncertain reliability and validity. We aimed to identify the underlying rules to enable documentation, review, and future use of these expert-based exposure decisions.
Classification and regression trees (CART, predictions from a single tree) and random forests (predictions from many trees) were used to identify the underlying rules from the questionnaire responses and an expert's exposure assignments for occupational diesel exhaust exposure for several metrics: binary exposure probability and ordinal exposure probability, intensity, and frequency. Data were split into training (n=10,488 jobs), testing (n=2,247), and validation (n=2,248) data sets.
The CART and random forest models' predictions agreed with 92–94% of the expert's binary probability assignments. For ordinal probability, intensity, and frequency metrics, the two models extracted decision rules more successfully for unexposed and highly exposed jobs (86–90% and 57–85%, respectively) than for low or medium exposed jobs (7–71%).
CART and random forest models extracted decision rules and accurately predicted an expert's exposure decisions for the majority of jobs and identified questionnaire response patterns that would require further expert review if the rules were applied to other jobs in the same or different study. This approach makes the exposure assessment process in case-control studies more transparent and creates a mechanism to efficiently replicate exposure decisions in future studies.
diesel exhaust; classification; data mining; occupational exposure
Animal evidence suggests that circadian disruption may be associated with ovarian cancer, though very little epidemiologic work has been done to assess this potential association. We evaluated the association between self-reported nightshift work, a known circadian disruptor, and ovarian cancer in a population-based case-control study.
The study included 1,101 women with invasive epithelial ovarian cancer, 389 women with borderline epithelial ovarian tumors and 1,832 controls and was conducted in Western Washington State. Shift work data was collected as part of in-person interviews.
Working the nightshift was associated with an increased risk of invasive (OR=1.24, 95% CI: 1.04–1.49) and borderline (OR=1.48, 95% CI: 1.15–1.90) tumors; however, we observed little evidence that risks increased with increasing cumulative duration of nightshift work, and risks were not elevated in the highest duration category (>7 nightshift work-years). Increased risks were restricted to women who were 50 years of age and older and to serous and mucinous histologies of invasive and borderline tumors. There was suggestive evidence of a decreased risk of ovarian cancer among women reporting a preference for activity during evenings rather than mornings.
We found evidence suggesting an association between shift work and ovarian cancer. This observation should be followed up in future studies incorporating detailed assessments of diurnal preference (i.e. chronotype) in addition to detailed data on shift schedules.
shift work; ovarian cancer; circadian; chronotype
Chronic low level exposure of agricultural workers and applicators to pesticides has been found to be associated with different degrees of decrement in cognitive and psychomotor functions. The goal of this study was to use meta-analysis to (1) identify and quantify neurobehavioral deficits among agricultural workers and pesticide applicators, and (2) analyse the potential confounders or moderators of these neurobehavioral deficits. Seventeen studies, reporting on 21 independent cohort groups, were included in the meta-analysis. These studies involved 16 neuropsychological tests providing 23 different performance measures that constitute the neurobehavioral constructs. All tests and measures of the neurobehavioral functions of attention, visuomotor integration, verbal abstraction and perception constructs showed significant decrements for exposed participants. One out of three tests of memory, two of five tests of sustained attention, and four of eight tests of motor speed constructs also showed significant decrements. Nine out of these 15 effect size distributions demonstrated significant heterogeneity across cohorts. A search for cohort-level variables (eg, agricultural workers vs applicators, duration of exposure, age and percentage of male participants) to explain this heterogeneity was largely unsuccessful. However, for one test, Block Design, the duration of exposure was positively associated with performance decrements. Furthermore, it was also found that performance decrements on this test were smaller for older participants. Increasing the number of studies and using more consistent methodologies in field studies are needed.
Recent investigations have associated airborne Particulate Matter (PM) with increased coagulation and thrombosis, but underlying biological mechanisms are still incompletely characterized. 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-characterized 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 Endogenous Thrombin Potential (ETP), as a global coagulation-activation test after standardized triggers.
ETP increased in association with PM10 (β=20.0, 95%CI: 3.0, 37.0), PM1 (β=80.8 95%CI: 14.9, 146.7), and zinc (β=51.3, 95%CI: 0.01, 111.1) exposures. NOS3 methylation was negatively associated with PM10 (β=−0.2, 95%CI: −0.4, −0.03), PM1 (β=−0.8, 95%CI: −1.4, −0.1), zinc (β=−0.9, 95%CI: −1.4, −0.3) and iron (β=−0.7, 95%CI: −1.4, −0.01) exposures. Zinc exposure was negatively associated with EDN1 (β=−0.3, 95%CI: −0.8, −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.
Air pollution; DNA methylation; coagulation
To quantify the variation in rates of absence for musculoskeletal pain across 47 occupational groups (mostly nurses and office workers) from 18 countries, and to explore personal and group-level risk factors that might explain observed differences.
A standardised questionnaire was used to obtain information about musculoskeletal pain, sickness absence and possible risk factors in a cross-sectional survey of 12,416 workers (92 to 1017 per occupational group). In addition, group-level data on socioeconomic variables such as sick pay and unemployment rates were assembled by members of the study team in each country. Associations of sickness absence with risk factors were examined by Poisson regression.
Overall, there were more than 30-fold differences between occupational groups in the 12-month prevalence of prolonged musculoskeletal sickness absence, and even among office workers carrying out similar occupational tasks, the variation was more than ten-fold. Personal risk factors included older age, lower educational level, tendency to somatise, physical loading at work and prolonged absence for non-musculoskeletal illness. However, these explained little of the variation between occupational groups. After adjustment for individual characteristics, prolonged musculoskeletal sickness absence was more frequent in groups with greater time pressure at work, lower job control, and more adverse beliefs about the work-relatedness of musculoskeletal disorders.
Musculoskeletal sickness absence might be reduced by eliminating excessive time pressures in work, maximising employees’ responsibility and control, and providing flexibility of duties for those with disabling symptoms. Care should be taken not to overstate work as a cause of musculoskeletal injury.
Sickness absence; musculoskeletal; international; risk factors; time pressure; job control
Chlorinated solvents are classified as probable or possible carcinogens. It is unknown whether exposure to these agents increases the risk of malignant or benign brain tumors. Our objective was to evaluate associations of brain tumor risk with occupational exposure to six chlorinated solvents [i.e., dichloromethane, chloroform, carbon tetrachloride, 1,1,1-trichloroethane, trichloroethylene, and perchloroethylene].
489 glioma cases, 197 meningioma cases, and 799 controls were enrolled in a hospital-based case-control study conducted at three U.S. hospitals in Arizona, Massachusetts and Pennsylvania. Information about occupational history was obtained through a detailed in-person interview that included job-specific modules of questions such that the interview was tailored to each individual’s particular work history. An industrial hygienist assessed potential solvent exposure based on this information and an exhaustive review of the relevant industrial hygiene literature. Unconditional logistic regression models were used to calculate odds ratios (OR) and 95% confidence intervals (95%CI) for each solvent for ever/never, duration, cumulative, average weekly, and highest exposure.
Overall, we found no consistent evidence of an increased risk of glioma or meningioma related to occupational exposure to the six chlorinated solvents evaluated. There was some suggestion of an association between carbon tetrachloride and glioma in analyses restricted to exposed subjects, with average weekly exposure above the median associated with increased risk compared to below-median exposure (OR=7.1, 95%CI: 1.1, 45.2).
We found no consistent evidence for increased brain tumor risk related to chlorinated solvents.
epidemiology; cancer; solvents
There is great interest in evaluating gene-environment interactions with chemical exposures, but exposure assessment poses a unique challenge in case-control studies. Expert assessment of detailed work history data is usually considered the best approach, but it is a laborious and time-consuming process. We set out to determine if a less intensive method of exposure assessment (a job exposure matrix [JEM]) would produce similar results to a previous analysis that found evidence of effect modification between expert assessed-lead exposure and risk of brain tumors by a single nucleotide polymorphism in the ALAD gene (rs1800435).
We used data from a study of 355 patients with glioma, 151 patients with meningioma and 505 controls. Logistic regression models were used to examine associations between brain tumor risk and lead exposure and effect modification by genotype. We evaluated Cohen’s kappa, sensitivity and specificity for the JEM compared to the expert-assessed exposure metrics.
Although effect estimates were imprecise and driven by a small number of cases, we found evidence of effect modification between lead exposure and ALAD genotype when using expert- but not JEM-derived lead exposure estimates. Kappa values indicated only modest agreement (< 0.5) for the exposure metrics, with the JEM indicating high specificity (~0.9) but poor sensitivity (~0.5). Disagreement between the two methods was generally due to having additional information in the detailed work history.
These results provide preliminary evidence suggesting that high quality exposure data are likely to improve the ability to detect genetic effect modification.
Because of their high prevalence in the general population, genetic variants that determine susceptibility to environmental exposures may contribute greatly to the development of occupational diseases in the setting of specific exposures occurring in the workplace. Studies investigating genetic susceptibilities in the workplace may: (1) provide mechanistic insight into the aetiology of disease, in particular the determination of environmentally responsive genes; (2) identify susceptible subpopulations with respect to exposure; and (3) provide valuable input in setting occupational exposure limits by taking genetic susceptibility into account. Polymorphisms in the NAT2 and the HLA-DPB1Glu69 genes provide classic examples of how genetic susceptibility markers have a clear role in identifying disease risk in bladder cancer and chronic beryllium disease, respectively. For diseases with more complex and multifactorial aetiology such as occupational asthma and chronic airways disease, susceptibility studies for selected genetic polymorphisms provide additional insight into the biological mechanisms of disease. Even when polymorphisms for genetic susceptibility have a clear role in identifying disease risk, the value of wide scale genetic screening in occupational settings remains limited due to primarily ethical and social concerns. Thus, large scale genetic screening in the workplace is not currently recommended.
To determine if the GSTM1 null genotype is a risk factor for increased inflammatory response to inhaled endotoxin.
35 volunteers who had undergone inhalation challenge with a 20 000 endotoxin unit dose of Clinical Center Reference Endotoxin (CCRE) were genotyped for the GSTM1 null polymorphism. Parameters of airway and systemic inflammation observed before and after challenge were compared in GSTM1 null (n=17) and GSTM1 (n=18) sufficient volunteers.
GSTM1 null volunteers had significantly increased circulating white blood cells (WBCs), polymorphonuclear neutrophils (PMNs), platelets and sputum PMNs (% sputum PMNs and PMNs/mg sputum) after CCRE challenge. GSTM1 sufficient volunteers had significant, but lower increases in circulating WBCs, PMNs and % sputum PMNs, and no increase in platelets or PMNs/mg sputum. Linear regression analysis adjusted for baseline values of the entire cohort revealed that the GSTM1 null genotype significantly increased circulating WBCs, platelets and % sputum PMNs after challenge
These data support the hypothesis that the GSTM1 null genotype is a risk factor for increased acute respiratory and systemic inflammatory response to inhaled CCRE. These data are consistent with other observations that the GSTM1 null genotype is associated with increased respiratory, systemic and cardiovascular effects linked to ambient air particulate matter exposure and indicate that the GSTM1 null genotype should be considered a risk factor for adverse health effects associated with exposure to environmental endotoxin.
Although occupational exposure to cotton dust and endotoxin is
associated with adverse respiratory health, associations with cancer are
unclear. We investigated cancer mortality in relation to cotton dust and
endotoxin exposure in the Shanghai textile workers cohort.
We followed 444 cotton textile and a reference group of 467 unexposed
silk workers for 30 years (26 777 person-years). HRs for all cancers
combined (with and without lung cancer) and gastrointestinal cancer were
estimated in Cox regression models as functions of cotton textile work and
categories of cumulative exposure (low, medium, high), after adjustment for
covariates including pack-years smoked. Different lag years accounted for
Risks of mortality from gastrointestinal cancers and all cancers
combined, with the exclusion of lung cancer, were increased in cotton
workers relative to silk workers. When stratified by category of cumulative
cotton exposure, in general, risks were greatest for 20-year lagged medium
exposure (all cancers HR=2.7 (95% CI 1.4 to 5.2); cancer excluding lung
cancer HR=3.4 (1.7–7.0); gastrointestinal cancer HR=4.1
(1.8–9.7)). With the exclusion of lung cancer, risks of cancer were
more pronounced. When stratified by category of cumulative endotoxin
exposure, consistent associations were not observed for all cancers
combined. However, excluding lung cancer, medium endotoxin exposure was
associated with all cancers and gastrointestinal cancer in almost all lag
Cotton dust may be associated with cancer mortality, especially
gastrointestinal cancer, and endotoxin may play a causative role. Findings
also indirectly support a protective effect of endotoxin on lung cancer.
Professional judgment is necessary to assess occupational exposure in population-based case-control studies; however, the assessments lack transparency and are time-consuming to perform. To improve transparency and efficiency, we systematically applied decision rules to the questionnaire responses to assess diesel exhaust exposure in the New England Bladder Cancer Study, a population-based case-control study.
2,631 participants reported 14,983 jobs; 2,749 jobs were administered questionnaires (‘modules’) with diesel-relevant questions. We applied decision rules to assign exposure metrics based solely on the occupational history responses (OH estimates) and based on the module responses (module estimates); we combined the separate OH and module estimates (OH/module estimates). Each job was also reviewed one at a time to assign exposure (one-by-one review estimates). We evaluated the agreement between the OH, OH/module, and one-by-one review estimates.
The proportion of exposed jobs was 20–25% for all jobs, depending on approach, and 54–60% for jobs with diesel-relevant modules. The OH/module and one-by-one review had moderately high agreement for all jobs (κw=0.68–0.81) and for jobs with diesel-relevant modules (κw=0.62–0.78) for the probability, intensity, and frequency metrics. For exposed subjects, the Spearman correlation statistic was 0.72 between the cumulative OH/module and one-by-one review estimates.
The agreement seen here may represent an upper level of agreement because the algorithm and one-by-one review estimates were not fully independent. This study shows that applying decision-based rules can reproduce a one-by-one review, increase transparency and efficiency, and provide a mechanism to replicate exposure decisions in other studies.
Environmental exposure to multiple metals is common. A number of metals cause nephrotoxicity with acute and/or chronic exposure. However, few epidemiologic studies have examined the impact of metal co-exposure on kidney function. Therefore, we evaluated associations of antimony and thallium with kidney outcomes and assessed the impact of cadmium exposure on those associations in lead workers.
Multiple linear regression was used to examine associations between ln-urine thallium, antimony and cadmium levels with serum creatinine- and cystatin-C-based glomerular filtration measures, and ln-urine N-acetyl-β-D-glucosaminidase (NAG).
In 684 participants, median urine thallium and antimony were 0.39 and 0.36 μg/g creatinine, respectively. After adjustment for lead dose, urine creatinine, and kidney risk factors, higher ln-urine thallium was associated with higher serum creatinine- and cystatin-C-based estimates of glomerular filtration rate (eGFR); associations remained significant after adjustment for antimony and cadmium (regression coefficient for serum creatinine-based eGFR = 5.2 mL/min/1.73 m2; 95% confidence interval = 2.4, 8.0). Antimony associations with kidney outcomes were attenuated by thallium and cadmium adjustment; thallium and antimony associations with NAG were attenuated by cadmium.
Urine thallium levels were significantly associated with both serum creatinine- and cystatin-C-based glomerular filtration measures in a direction opposite that expected with nephrotoxicity. Given similarities to associations recently observed with cadmium, these results suggest that interpretation of urine metal values, at exposure levels currently present in the environment, may be more complex than previously appreciated. These results also support multiple metal analysis approaches to decrease the potential for inaccurate risk conclusions.
antimony; cadmium; creatinine; kidney function; thallium
We assessed the evidence relating pre-term delivery (PTD), low birthweight, small for gestational age (SGA), pre-eclampsia and gestational hypertension to five occupational exposures (working hours, shift work, lifting, standing and physical workload). We conducted a systematic search in MEDLINE and EMBASE (1966–2011), updating a previous search with a further six years of observations.
As before, combinations of keywords and MeSH terms were used. Each relevant paper was assessed for completeness of reporting and potential for important bias or confounding, and its effect estimates abstracted. Where similar definitions of exposure and outcome existed we calculated pooled estimates of relative risk in meta-analysis.
Analysis was based on 86 reports (32 cohort investigations, 57 with usable data on PTD, 54 on birthweight and 11 on pre-eclampsia/gestational hypertension); 33 reports were new to this review. For PTD, findings across a substantial evidence base were generally consistent, effectively ruling out large effects (e.g. RR>1.2). Larger and higher quality studies were less positive, while meta-estimates of risk were smaller than previously and best estimates pointed to modest or null effects (RR 1.04 to 1.18). For SGA, the position was similar but meta-estimates were even closer to the null (eight of nine RRs ≤ 1.07). For pre-eclampsia/gestational hypertension the evidence base remains insufficient.
The balance of evidence is against large effects for the associations investigated. As the evidence base has grown, estimates of risk in relation to these outcomes have become smaller.
pregnancy; occupation; review; meta-analysis
Studies show that exposure to air pollution damages human health, but the mechanisms are not fully understood. One suggested pathway is via oxidative stress.
This study is to examine associations between exposure to air pollution and oxidative DNA damage, as indicated by urinary 8-hydroxy-2’-deoxyguanosine (8-OHdG) concentrations in aging participants during 2006-2008.
We fit linear regression models to examine associations between air pollutants and 8-OHdG adjusting for potential confounders.
8-OHdG was significantly associated with ambient particulate matter ≤ 2.5 μm in aerodynamic diameter (PM2.5), the number of particles (PN), nitrogen dioxide (NO2), maximal 1-hour ozone (O3), sulfate (SO42-) and organic carbon (OC), but not with black carbon (BC), carbon monoxide (CO) or elemental carbon (EC). Effects were more apparent with multi-week averages of exposures. Per IQR increases of 21-day averages of PM2.5, PN, BC, EC, OC, CO, SO42-, NO2 and maximal 1-hour O3 were associated with 30.8% (95% confidence interval (CI): 9.3%, 52.2%), -13.1% (95%CI: -41.7%, 15.5%), 3.0% (95% CI: -19.8%, 25.8%), 5.3% (95% CI: -23.6%, 34.2%), 24.4% (95% CI: 1.8%, 47.1%), -2.0% (95% CI: -12.4%, 8.3%), 29.8% (95% CI: 6.3%, 53.3%), 32.2% (95% CI: 7.4%, 56.9%) and 47.7% (95% CI: 3.6%, 91.7%) changes in 8-OHdG, respectively.
This study suggests that aging participants experienced an increased risk of developing oxidative DNA injury after exposure to the secondary, but not primary ambient pollutants.
8-Hydroxy-2′-Deoxyguanosine; air pollution; DNA damage; oxidative stress; biomarker
Several epidemiologic studies have suggested that certain paternal occupations may be associated with an increased prevalence of birth defects in offspring. Using data from the National Birth Defects Prevention Study, we investigated the association between paternal occupation and birth defects in a case-control study of cases comprising over 60 different types of birth defects (n = 9998) and non-malformed controls (n = 4066) with dates of delivery between 1997 and 2004.
Using paternal occupational histories reported by mothers via telephone interview, jobs were systematically classified into 63 groups based on shared exposure profiles within occupation and industry. Data were analyzed using Bayesian logistic regression with a hierarchical prior for dependent shrinkage to stabilize estimation with sparse data.
Several occupations were associated with an increased prevalence of various birth defect categories, including: mathematical, physical and computer scientists; artists; photographers and photo processors; food service workers; landscapers and groundskeepers; hairdressers and cosmetologists; office and administrative support workers; sawmill workers; petroleum and gas workers; chemical workers; printers; material moving equipment operators; and motor vehicle operators.
Findings from this study might be used to identify specific occupations worthy of further investigation, and to generate hypotheses about chemical or physical exposures common to such occupations.
Bayes theorem; congenital abnormalities; occupational exposure; occupations; paternal exposure
Occupational noise-induced hearing loss (NIHL) is prevalent, yet evidence on the effectiveness of preventive interventions is lacking. The effectiveness of a new technology allowing workers to monitor daily at-ear noise exposure was analysed.
Workers in the hearing conservation program of an aluminium smelter were recruited because of accelerated rates of hearing loss. The intervention consisted of daily monitoring of at-ear noise exposure and regular feedback on exposures from supervisors. The annual rate of change in high frequency hearing average at 2, 3 and 4 KHz before intervention (2000–2004) and 4 years after intervention (2006–2009) was determined. Annual rates of loss were compared between 78 intervention subjects and 234 controls in other company smelters matched for age, gender and high frequency hearing threshold level in 2005.
Individuals monitoring daily noise exposure experienced on average no further worsening of high frequency hearing (average rate of hearing change at 2, 3 and 4 KHz=–0.5 dB/year). Matched controls also showed decelerating hearing loss, the difference in rates between the two groups being significant (p<0.0001). Analysis of a subset of intervention subjects matched to controls for initial rate of hearing loss showed a similar trend but the difference was not statistically significant (p=0.06).
Monitoring daily occupational noise exposure inside hearing protection with ongoing administrative feedback apparently reduces the risk of occupational NIHL in industrial workers. Longer follow-up of these workers will help determine the significance of the intervention effect. Intervention studies for the prevention of NIHL need to include appropriate control groups.
To investigate cancer risk, particularly oesophageal cancer, among male upstream petroleum workers offshore potentially exposed to various carcinogenic agents.
Using the Norwegian Registry of Employers and Employees, 24 765 male offshore workers registered from 1981 to 2003 was compared with 283 002 male referents from the general working population matched by age and community of residence. The historical cohort was linked to the Cancer Registry of Norway and the Norwegian Cause of Death Registry.
Male offshore workers had excess risk of oesophageal cancer (RR 2.6, 95% CI 1.4 to 4.8) compared with the reference population. Only the adenocarcinoma type had a significantly increased risk (RR 2.7, 95% CI 1.0 to 7.0), mainly because of an increased risk among upstream operators (RR 4.3, 95% CI 1.3 to 14.5). Upstream operators did not have significant excess of respiratory system or colon cancer or mortality from any other lifestyle-related diseases investigated.
We found a fourfold excess risk of oesophageal adenocarcinoma among male workers assumed to have had the most extensive contact with crude oil. Due to the small number of cases, and a lack of detailed data on occupational exposure and lifestyle factors associated with oesophageal adenocarcinoma, the results must be interpreted with caution. Nevertheless, given the low risk of lifestyle-related cancers and causes of death in this working group, the results add to the observations in other low-powered studies on oesophageal cancer, further suggesting that factors related to the petroleum stream or carcinogenic agents used in the production process might be associated with risk of oesophageal adenocarcinoma.
Though toxicological experiments demonstrate the teratogenicity of organic solvents in animal models, epidemiologic studies have reported inconsistent results. Using data from the population-based National Birth Defects Prevention Study, we examined the relation between maternal occupational exposure to aromatic solvents, chlorinated solvents and Stoddard solvent during early pregnancy and neural tube defects (NTDs) and orofacial clefts (OFCs).
Cases of NTDs (anencephaly, spina bifida and encephalocele) and OFCs (cleft lip ± cleft palate and cleft palate alone) delivered between 1997 and 2002 were identified by birth defect surveillance registries in 8 states; non-malformed control infants were selected using birth certificates or hospital records. Maternal solvent exposure was estimated by industrial hygienist review of self-reported occupational histories in combination with a literature-derived exposure database. Odds ratios (OR) and 95% confidence intervals (CI) for the association between solvent class and each birth defect group and component phenotype were estimated using multivariable logistic regression, adjusting for maternal age, race/ethnicity, education, pre-pregnancy body mass index, folic acid supplement use and smoking.
The prevalence of exposure to any solvent among mothers of NTD cases (n=511), OFC cases (n=1163) and controls (n=2977) was 13.1%, 9.6% and 8.2%, respectively. Exposure to chlorinated solvents was associated with increased odds of NTDs (OR=1.96; CI=1.34, 2.87), especially spina bifida (OR=2.26; CI=1.44, 3.53). No solvent class was strongly associated with OFCs in these data.
Our findings suggest that maternal occupational exposure to chlorinated solvents during early pregnancy is positively associated with the prevalence of NTDs in offspring.
congenital abnormalities; occupational exposure; solvents
Studies have shown greater health risks associated with blue-collar manufacturing employment for women than men. It remains challenging, however, to distinguish cultural gendered factors influencing employment decisions (e.g., expected work roles, family responsibilities) from sex-linked biological differences shaping physiological response to workplace physical hazards.
We examined effects of hourly (blue-collar) status on incident hypertension among men and women, using health claims data for 14,618 white- and blue-collar aluminum manufacturing employees in eight U.S. states. To explore gender differences in job status, we developed sex-stratified propensity score models identifying key socioeconomic predictors of hourly status for men and women. To examine effects of hourly employment on hypertension risk, after adjusting for gender differences in job placement, we applied time-weighted logistic regression models, stratified by propensity score, with additional adjustment for socioeconomic confounders.
Family structure (partnership, parity) influenced job status for both sexes; single mothers were more likely to hold hourly jobs (OR = 2.02 (95% CI = 1.37–2.97)), partnered men with children less likely (OR = 0.68 (0.56–0.83)). Education, age at hire, and race influenced job placement for both sexes. The effect of hourly status on hypertension was significant only among women predicted to be hourly (OR = 1.78 (1.34 – 2.35)).
Our results indicate significant risks of hypertension associated with hourly status for women, possibly exacerbated by sociodemographic factors predicting hourly status (e.g., single parenthood, low education). Greater attention to gender differences in job status, workplace stressors, and health risks associated with hourly work, is warranted.
Gender; sex; hourly status; hypertension; propensity scores