Using job exposure matrices to estimate an individual's exposure for compensation?

<h3>Introduction</h3> Job exposure matrices are being used to assign (quantitative levels of) exposure to individuals based on their job history. In human observational studies a group-based approach in which every individual with a similar job will be assigned similar exposure will not bias the exposure-response association but will result in loss of precision. However, since job exposure matrices do not consider between-worker differences in average exposure some workers’ cumulative exposures will be underestimated. This may affect their chances for compensation when a minimal (cumulative) exposure threshold is applied. <h3>Material and Methods</h3> We analysed more than 80.000 repeated exposure measurements from a variety of industries and consequently combined variance components of location and worker (within a location within a job) to estimate the bandwidth of individual average exposures in a job. This allowed estimation of an upper average exposure for workers within a job (across locations/companies). <h3>Results</h3> The bandwidth factor appeared to be larger for exposures to particulates than for gases. It was also larger for biological agents. For exposure to particulate matter the bandwidth factor varied slightly between industries (84BWfactor 1-4) with a median of 2.5. <h3>Conclusion</h3> By applying a default upper (one standard deviation) bandwidth factor to an average exposure estimate resulting from a job-exposure matrix, the Dutch occupational disease compensation scheme has chosen for an approach that recognizes between-worker differences in exposure. This approach in addition to considering uncertainty in exposure-response associations addresses another important factor of uncertainty in ascertaining occupational disease based on the ‘presumably plausible’ principle.

Authors' response to: Qualitative job-exposure matrix--a tool for the quantification of population-attributable fractions for occupational lung carcinogens?

Although a valuable method in occupational epidemiology, job-exposure -matrices are no magic fix.

Although polychlorinated biphenyls (PCBs) have been banned in many countries for more than three decades, exposures to PCBs continue to be of concern due to their long half-lives and carcinogenic effects. In National Institute for Occupational Safety and Health studies, we are using semiquantitative plant-specific job exposure matrices (JEMs) to estimate historical PCB exposures for workers (n = 24,865) exposed to PCBs from 1938 to 1978 at three capacitor manufacturing plants. A subcohort of these workers (n = 410) employed in two of these plants had serum PCB concentrations measured at up to four times between 1976 and 1989. Our objectives were to evaluate the strength of association between an individual worker's measured serum PCB levels and the same worker's cumulative exposure estimated through 1977 with the (1) JEM and (2) duration of employment, and to calculate the explained variance the JEM provides for serum PCB levels using (3) simple linear regression. Consistent strong and statistically significant associations were observed between the cumulative exposures estimated with the JEM and serum PCB concentrations for all years. The strength of association between duration of employment and serum PCBs was good for highly chlorinated (Aroclor 1254/HPCB) but not less chlorinated (Aroclor 1242/LPCB) PCBs. In the simple regression models, cumulative occupational exposure estimated using the JEMs explained 14-24% of the variance of the Aroclor 1242/LPCB and 22-39% for Aroclor 1254/HPCB serum concentrations. We regard the cumulative exposure estimated with the JEM as a better estimate of PCB body burdens than serum concentrations quantified as Aroclor 1242/LPCB and Aroclor 1254/HPCB.

ObjectivesExposure assessment for retrospective industrial cohorts are often hampered by limited availability of historical measurements. This study describes the development of company-specific job-exposure matrices (JEMs) based on measurements collected over...

The determination of cumulative exposures for individual workers is necessary for research and practice of occupational health and hygiene. Reconstruction of exposures for a study of respiratory morbidity was needed to study the effects of exposure to carbon black production. Approximately 15,800 exposure estimates were needed. There were 22 plants, a 40-year time span, six job categories, and three types of dust-exposure metrics (respirable, inhalable, and "total" dust). Three information sources were used: 1) Industrial hygiene air level measurements where available (several industry-wide surveys had been conducted). 2) A formal process survey identifying specific dates and types of process and control changes. 3) An Historical Relative Exposure Rating Scale; plant health and safety personnel used this spreadsheet-based rating scheme to quantify exposures before and between years of actual measurement relative to a reference year in which measurements were available. A job-exposure matrix was calculated by integrating these three methods. Linear scaling factors were identified to interconvert geometric to arithmetic means and to interconvert total and inhalable dust. Individual worker cumulative exposures were then calculated based upon job histories linked with the job-exposure matrix. The nine-step process for integrating all available relevant data was effective in estimating the exposures for each of the cells of the job-exposure matrix. Among the 1680 workers participating, the mean cumulative inhalable dust exposure was 48.4 mg-years/m3. Early years contribute disproportionately to the cumulative exposures of individuals since levels have declined significantly over time. The use of multiple sources of information, including a relative exposure rating instrument, significantly facilitates reconstruction of historical exposures. Inadequate adjustment for temporal trends can lead to underestimation of cumulative exposures and significantly affect estimation of dose-effect relationships. These methods are applicable to other situations requiring estimation of cumulative exposure with sparse industrial hygiene data in early years.

Occupational airway diseases are common among bakers. The present study describes the association between exposure to wheat allergen levels and sensitization to wheat allergens, work-related upper and lower respiratory symptoms and asthma in bakery workers. As part of a Health Surveillance System for early detection of (allergic) occupational airway diseases a so-called 'validation study' was performed among Dutch bakers for validation of a diagnostic model that predict the likelihood of sensitization to specific workplace allergens. The present study used serology and questionnaire results of a subgroup of 860 bakers participating in the validation study. An earlier developed job-exposure matrix was used to predict average and cumulative personal exposure to wheat allergens. The prevalence of wheat sensitization, work-related respiratory symptoms and asthma increased till average wheat exposure levels of approximately 25-30 microg/m3, leveled off and decreased at higher exposure concentrations. Exposure-response curves showed a stronger pronounced bell-shape with cumulative exposure. Associations were strongest for asthma and work-related lower respiratory symptoms (PR approximately 2 and PR approximately 3.5-4.5 for average and cumulative exposure, respectively). Associations were only found in atopics. Wheat sensitization was an important factor in the prevalence of respiratory symptoms. In accordance with earlier studies, the present study showed a bell-shaped exposure-response relationship especially for cumulative wheat allergen exposure with sensitization, allergic respiratory symptoms and asthma. The healthy worker effect may be the possible explanation for the bell-shaped relationship.

Tolerance of Pinus rigida trees to a ten-year exposure to chronic gamma irradiation from cobalt-60

RATIONALE: Job exposure matrices (JEMs) are widely used in occupational epidemiology, particularly when biological or environmental monitoring data are scanty. However, as with most exposure estimates, JEMs may be vulnerable...

BackgroundOccupational exposure to artificial stone, a popular material used for countertops, can cause accelerated silicosis, but the precise relationship between silica dose and disease development is unclear.ObjectivesThis study evaluated the impact of silica exposure on lung function and chest imaging in artificial stone manufacturing workers.MethodsQuestionnaire and spirometry assessments were administered to workers in two plants. A high-exposure subset underwent further evaluation, including chest CT and DLco. Weighting factors, assigned as proxies for silica exposure, were based on work tasks. Individual cumulative exposures were estimated using area concentration measurements and time spent in specific areas. Exposure-response associations were analyzed using linear and logistic regression models.ResultsAmong 65 participants, the mean cumulative silica exposure was 3.61 mg/m3-year (range 0.0001 to 44.4). Each 1 mg/m3-year increase was associated with a 0.46% reduction in FVC, a 0.45% reduction in FEV1, and increased lung function abnormality risk (aOR = 1.27, 95% CI = 1.03–1.56). Weighting factors correlated with cumulative exposures (Spearman correlation = 0.59, p < 0.0001), and weighted tenure was associated with lung function abnormalities (aOR = 1.04, 95% CI = 1.01–1.09). Of 37 high-exposure workers, 19 underwent chest CT, with 12 (63%) showing abnormal opacities. Combining respiratory symptoms, lung function, and chest X-ray achieved 91.7% sensitivity and 75% specificity for predicting chest CT abnormalities.ConclusionLung function and chest CT abnormalities occur commonly in artificial stone workers. For high-exposure individuals, abnormalities on health screening could prompt further chest CT examination to facilitate early silicosis detection.

We studied cancer mortality and mesothelioma incidence in 974 male workers employed at least 6 months at the Balangero mine (Italy), the largest chrysotile mine in Western Europe, active from 1917 to 1985. Vital status as of 31 May 2013, causes of deaths and mesothelioma incidence from 1990 were ascertained. Past exposure to asbestos by working area and calendar period was estimated, based on historical data of fibers concentrations. Individual cumulative exposure was assessed by applying estimates to the job history of cohort members. Standardized mortality ratios (SMRs) for selected causes and standardized incidence ratios for malignant mesothelioma (MM) were calculated based on regional reference rates. Poisson regression analysis was used to study MM and lung cancer risk by latency, duration, and cumulative exposure. Mortality was increased for all causes (SMR = 1.28; 95% confidence interval [CI] = 1.17-1.40), pleural cancer (SMR = 4.30; 95% CI = 1.58-9.37), asbestosis (SMR = 375.06; 95% CI = 262.68-519.23). An increase was also found for lung cancer (SMR = 1.14; 95% CI = 0.81-1.55) and peritoneal cancer (SMR = 3.25; 95% CI = 0.39-11.75). The risk of both pleural and peritoneal cancer mortality and of mesothelioma incidence increased with increasing cumulative exposure, duration, and latency. Poisson regression analyses showed an increase in mesothelioma risk with cumulative asbestos exposure and suggest a similar trend for lung cancer. Asbestosis mortality also increased with cumulative exposure. Among Balangero chrysotile miners and millers, the occurrence of malignant and nonmalignant asbestos-related diseases was increased by exposure, with dose-response relation. The study confirms the carcinogenicity of chrysotile asbestos, in particular for pleural mesothelioma.

Objectives: To evaluate potential confounding of the association between beryllium and lung cancer in a reanalysis of data from a published case–control study of workers at a beryllium processing facility....

Serum type III procollagen peptide (PIIIP), a degradation product of the type III collagen precursor, has been put forward as an exposure marker for mineral dust. We evaluated PIIIP levels as a marker of exposure to and effects of coal dust in retired coal miners (n = 104). To this end: (a) the individual cumulative dust exposure was calculated from job-exposure matrices, and (b) in addition to routine chest radiography (CR) of all miners according to the criteria of the International Labour Organisation (ILO), a subgroup (n = 46) was screened by high-resolution computed tomography (HRCT). Profusion score (CR and HRCT) tended to increase with cumulative dust exposure, even in the absence of CR evidence for pneumoconiosis (i.e. CR < or = 0/1, n = 35). In contrast to our previous findings in active miners, PIIIP levels were not increased in miners as compared with non-dust-exposed controls (n = 29), and no differences were observed between miners without (ILO = 0/0) and miners with coal workers' pneumoconiosis (CWP; ILO > or = 0/1). No trend in PIIIP versus pneumoconiosis stage was present, either by CR or by the more sensitive HRCT score. PIIIP was also unrelated to any lung function parameter (FEV1, FVC, impedance, diffusion capacity). Age, medication, medical history and smoking habits had no significant effect on PIIIP levels. In the miners with CWP (i.e. ILO > 0/0, n = 28) a significant negative correlation was present between PIIIP values and (log) cumulative dust exposure. This decrease in serum PIIIP levels with increasing cumulative exposure may be due to chronic adaptive changes in type III collagen deposition and/or breakdown. Other relations between exposure and PIIIP were not observed. In conclusion, the present findings do not support the use of serum type III procollagen peptide as a marker of exposure to and (early) interstitial or respiratory effects of coal dust.

Occupational exposure to respirable crystalline silica (RCS) has been associated with both silicosis and lung cancer, but no systematic review (SR) specifically focused on exposure-response relationships has been published for these diseases. We conducted this SR in compliance with Preferred Reporting Items for Systematic reviews and Meta-Analyses (PRISMA) guidelines. PubMed searches, supplemented with Web of Science and Google Scholar searches, identified 1,007 potentially relevant articles. After applying selection criteria and removing duplicates, 65 publications were reviewed and evaluated, 20 of which presented at least semi-quantitative exposure-response results for lung cancer (n = 12) and/or silicosis (n = 10). Cumulative RCS exposure was most commonly reported. Increasing silicosis risk with increasing cumulative RCS exposure was reported in all studies, with exposure thresholds indicated, but at different cumulative exposures. For most studies defining silicosis as International Labor Organization (ILO) score ≥ 1/0, substantially increased risks were clear at or above 1 mg-/m3-yr. For lung cancer, exposure-response estimates were mixed with 4 studies reporting no statistically significantly increased relative risk of lung cancer at any cumulative RCS exposure. Three studies reported statistically significant increased risks but only for high cumulative RCS exposures. Residual confounding by smoking was not explicitly discussed in most studies. One case-control study presented an exposure-response analysis for silica and lung cancer limited to never-smokers with substantial silica exposure; risk was increased only among those in the highest RCS exposure category. Studies with more detailed smoking information generally reported risks close to background levels except at the highest cumulative RCS exposure categories. Silicosis risk clearly and consistently was increased above cumulative exposure thresholds of roughly 1 mg/m3-years across most studies. However, for lung cancer, results were heterogeneous with potential residual confounding by smoking complicating interpretation. Results suggest that lung cancer risk may not be increased at cumulative RCS exposures below the reported exposure thresholds for silicosis risk.

Threshold Value Estimation for Respirable Quartz Dust Exposure and Silicosis Incidence Among Workers in the German Porcelain Industry