Characterization of perceived biohazard exposures, personal protective equipment, and training resources among a sample of formal U.S. solid waste workers: A pilot study.

In the United States, the majority of waste workers work with solid waste. In solid waste operations, collection, sorting, and disposal can lead to elevated biohazard exposures (e.g., bioaerosols, bloodborne and other pathogens, human and animal excreta). This cross-sectional pilot study aimed to characterize solid waste worker perception of biohazard exposures, as well as worker preparedness and available resources (e.g., access to personal protective equipment, level of training) to address potential biohazard exposures. Three sites were surveyed: (1) a family-owned, small-scale waste disposal facility, (2) a county-level, recycling-only facility, and (3) an industrial-sized, large-scale facility that contains a hauling and landfill division. Survey items characterized occupational biohazards, resources to mitigate and manage those biohazards, and worker perceptions of biohazard exposures. Descriptive statistics were generated. The majority of workers did not report regularly coming into contact with blood, feces, and bodily fluids (79%). As such, less than one-fifth were extremely concerned about potential illness from biological exposures (19%). Yet, most workers surveyed (71%) reported an accidental laceration/cut that would potentially expose workers to biohazards. This study highlights the need for additional research on knowledge of exposure pathways and perceptions of the severity of exposure among this occupational group.

Effort-Reward Imbalance among a Sample of Formal US Solid Waste Workers.

Background: Solid waste workers are exposed to a plethora of occupational hazards and may also experience work-related stress. Our study had three specific hypotheses: (1) waste workers experience effort−reward imbalance (ERI) with high self-reported effort but low reward, (2) unionized workers experience greater ERI, and (3) workers with higher income have lower ERI. Methods: Waste workers from three solid waste sites in Michigan participated in this cross-sectional study. We characterized perceived work stress using the short-version ERI questionnaire. Descriptive statistics and linear tests for trend were assessed for each scale. Linear regression models were constructed to examine the relationship between structural factors of work stress and ERI. Gradient-boosted regression trees evaluated which factors of effort or reward best characterize workers' stress. Results: Among 68 participants, 37% of workers reported high effort and low reward from work (ERI > 1). Constant pressure due to heavy workload was most indicative of ERI among the solid waste workers. Union workers experienced 79% times higher ERI than non-unionized workers, while no significant differences were observed by income, after adjusting for confounders. Conclusions: Organizational-level interventions, such as changes related to workload, consideration of fair compensation, and increased support from supervisors, can decrease work stress.

Oxidative stress and genotoxicity of co-exposure to chlorpyrifos and aflatoxin B1 in HepG2 cells.

Chlorpyrifos (CPF) and aflatoxin B1 (AFB1) are each known to adversely affect hepatic tissue individually, but their combined hepatic effects have never been previously investigated. HepG2 cell viability, oxidative status, and genetic impairment were examined after exposing HepG2 cells to: (1) CPF alone, (2) AFB1 alone, and (3) CPF and AFB1 combined (20:1). CPF exposure decreased cell viability, reduced glutathione (GSH) content, and superoxide dismutase (SOD) activity but increased both glutathione peroxidase (GPx) and paraoxonase 1 activity. AFB1 exposure decreased cell viability and GSH content but increased reactive oxygen species (ROS) production. CPF and AFB1 combined exposure decreased GSH content (p < 0.05) further over individual CPF and AFB1 exposures. Induction of micronucleus formation was detected in AFB1-treated cells but undetected in both CPF and combination-treated cells. In conclusion, cytotoxic effects caused by combined exposure were antagonistic, as shown by a combination index value of 1.67. Although no change in ROS production was observed in CPF groups, the overall results confirmed the occurrence of oxidative stress through the alterations of GSH content, GPx, and SOD activity. Only intracellular GSH was evidently changed upon exposure to CPF and AFB1 combined. Thus, this study suggested cellular GSH as a potential indicator for detecting the combined effects of CPF and AFB1 in HepG2 cells, the detection of which could be adapted to estimate the potential toxicity of additional multiple toxicant exposures.