No abstract

Purpose of Review We offer an in-depth discussion of the time-varying confounding and selection bias mechanisms that give rise to the healthy worker survivor effect (HWSE). Recent Findings In this update of an earlier review, we distinguish between the mechanisms collectively known as the HWSE and the statistical bias that can result. This discussion highlights the importance of identifying both the target parameter and the target population for any research question in occupational epidemiology. Target parameters can correspond to hypothetical workplace interventions; we explore whether these target parameters’ true values reflect the etiologic effect of an exposure on an outcome or the potential impact of enforcing an exposure limit in a more realistic setting. If a cohort includes workers hired before the start of follow-up, HWSE mechanisms can limit the transportability of the estimates to other target populations. Summary We summarize recent publications that applied g-methods to control for the HWSE, focusing on their target parameters, target populations, and hypothetical interventions.

Fine particulate matter (PM2.5) in air pollution, primarily from combustion sources, is recognized as an important risk factor for cardiovascular events but studies of workplace PM2.5 exposure are rare. We conducted a prospective study of exposure to PM2.5 and incidence of ischemic heart disease (IHD) in a cohort of 11,966 US aluminum workers. Incident IHD was identified from medical claims data from 1998 to 2008. Quantitative metrics were developed for recent exposure (within the last year) and cumulative exposure; however, we emphasize recent exposure in the absence of interpretable work histories prior to follow-up. IHD was modestly associated with recent PM2.5 overall. In analysis restricted to recent exposures estimated with the highest confidence, the hazard ratio (HR) increased to 1.78 (95%CI: 1.02, 3.11) in the second quartile and remained elevated. When the analysis was stratified by work process, the HR rose monotonically to 1.5 in both smelter and fabrication facilities, though exposure was almost an order of magnitude higher in smelters. The differential exposure-response may be due to differences in exposure composition or healthy worker survivor effect. These results are consistent with the air pollution and cigarette smoke literature; recent exposure to PM2.5 in the workplace appears to increase the risk of IHD incidence.

Marginal structural models (MSMs) and inverse probability weighting can be used to estimate risk in a cohort of active workers if there is a time-varying confounder (e.g., health status) affected by prior exposure-a feature of the healthy worker survivor effect. We applied Cox MSMs in a study of incident ischemic heart disease and exposure to particulate matter with aerodynamic diameter of 2.5 μm or less (PM2.5) in a cohort of 12,949 actively employed aluminum workers in the United States. The cohort was stratified by work process into workers in smelting facilities, herein referred to as "smelters" and workers in fabrication facilities, herein referred to as "fabricators." The outcome was assessed by using medical claims data from 1998 to 2012. A composite risk score based on insurance claims was treated as a time-varying measure of health status. Binary PM2.5 exposure was defined by the 10th-percentile cutoff for each work process. Health status was associated with past exposure and predicted the outcome and subsequent exposure in smelters but not in fabricators. In smelters, the Cox MSM hazard ratio comparing those always exposed above the cutoff with those always exposed below the cutoff was 1.98 (95% confidence interval: 1.18, 3.32). In fabricators, the hazard ratio from a traditional Cox model was 1.34 (95% confidence interval: 0.98, 1.83). Results suggest that occupational PM2.5 exposure increases the risk of incident ischemic heart disease in workers in both aluminum smelting and fabrication facilities.

No abstract

ObjectiveTo assess produce availability, quality and price in a large sample of food stores in low-income neighbourhoods in California.DesignCross-sectional statewide survey.SettingBetween 2011 and 2015, local health departments assessed store type, WIC (Supplemental Nutrition Program for Women, Infants, and Children)/SNAP (Supplemental Nutrition Assistance Program) participation, produce availability, quality and price of selected items in stores in low-income neighbourhoods. Secondary data provided reference chain supermarket produce prices matched by county and month. t Tests and ANOVA examined differences by store type; regression models examined factors associated with price.SubjectsLarge grocery stores (n 231), small markets (n 621) and convenience stores (n 622) in 225 neighbourhoods.ResultsProduce in most large groceries was rated high quality (97 % of fruits, 98 % of vegetables), but not in convenience stores (25 % fruits, 14 % vegetables). Small markets and convenience stores participating in WIC and/or SNAP had better produce availability, variety and quality than non-participating stores. Produce prices across store types were, on average, higher than reference prices from matched chain supermarkets (27 % higher in large groceries, 37 % higher in small markets, 102 % higher in convenience stores). Price was significantly inversely associated with produce variety, adjusting for quality, store type, and SNAP and WIC participation.ConclusionsThe study finds that fresh produce is more expensive in low-income neighbourhoods and that convenience stores offer more expensive, poorer-quality produce than other stores. Variety is associated with price and most limited in convenience stores, suggesting more work is needed to determine how convenience stores can provide low-income consumers with access to affordable, high-quality produce. WIC and SNAP can contribute to the solution.

Supplemental Digital Content is available in the text.

This is the final part of a study carried out to investigate occupational asthma due to sensitivity to colophony fumes (a component of soldering flux) in an electronics factory. Fifty-eight workers with occupational asthma employed on the main shop floor were investigated. In them the interval between first exposure and sensitisation varied widely with a group becoming sensitive within one to two years of first exposure, and another group whose sensitisation was delayed for three to 23 years. Once sensitised the interval between arriving at work and the onset of daily symptoms seemed to be bimodally distributed, resembling the immediate and late asthmatic symptoms seen on provocation testing. Twenty-three out of 58 had no definite daily deterioration at work but improved at the weekends. Wheeze and breathlessness occurred in the evenings at home in most, and one-third were woken by breathlessness at least on some nights. These 58 cases were compared with 48 controls without occupational asthma who had worked on the same shop floor for at least four years. Mean levels of FEV1 were significantly worse in the cases before exposure on Monday morning. The cases also had more than twice as much sickness absence as controls. FEV1 fell by more than 10% over a working shift in 33% of cases and 5% of controls. Atopy (a positive skin prick test to one or more common allergens) and a past history of allergic disease were weakly but significantly associated with being a case. The effects of smoking and a family history of allergic disease were trivial. Prick testing with an antigen derived from the colophony in the solder flux was completely negative, but cases and controls had significantly raised levels of total IgM compared with blood bank controls, perhaps suggesting some previously unrecognised immunological process.