Unionisation and injury risk in construction: a replication study.

OBJECTIVE: To replicate, in a more recent time period, a previous cross-sectional study to estimate the association between unionisation and the risk of workers' compensation injury claims. METHODS: The sampling frame was workers' compensation company account records in the industrial, commercial and institutional construction sector in the province of Ontario, Canada, 2012-2018. Company unionisation status was determined through linkage with records of unionised contractors. Outcomes were cumulative counts of workers' compensation injury claims, aggregated to company business. Risk ratios were estimated with multivariable negative binomial regression models. Models were also fit separately to lost-time claims stratified by company size. RESULTS: Business unionisation was associated with a lower lost-time claim incidence (crude risk ratio, CRR=0.69, 95% CI 0.65 to 0.74); adjusted risk ratio, ARR=0.75, 95% CI 0.71 to 0.80). In subgroup analyses, the magnitude of the ARR declined as company size decreased and was not statistically significant for the smallest-sized companies of ≤4 full-time equivalent employees. Unionisation was associated (positively) with the incidence of no-lost-time claims in a crude model, but not in an adjusted one (CRR=1.80, 95% CI 1.71 to 1.89; ARR=1.04, 95% CI 0.98 to 1.09). CONCLUSIONS: Company unionisation was associated with a lower risk of lost-time workers' compensation injury claims, corroborating a similar study from an earlier time period. The protective effect of unionisation declined as company size decreased. In contrast to the previous study, a positive relationship between company unionisation and no-lost-time claim incidence was not found, due in part to a methodological refinement.

Protecting Construction Worker Health and Safety in Ontario, Canada: Identifying a Union Safety Effect.

OBJECTIVES: Do Ontario unionized construction firms have lower workers' compensation claims rates compared with nonunion firms? METHODS: Building trade and construction trade association lists of union contractors were linked to Workplace Safety and Insurance Board claims data for 2006 to 2012. Data were pooled for 2006 to 2012, and negative binomial regressions conducted with adjustment to estimate a union safety effect. RESULTS: The sample included 5797 unionized and 38,626 nonunion construction firms. Total claims rates were 13% higher (1.13, 1.09 to 1.18) in unionized firms because of higher allowed no-lost-time claim rates (1.28, 1.23 to 1.34), whereas the lost-time claims rate was 14% lower (0.86, 0.82 to 0.91). CONCLUSIONS: Unionized construction firms compared with nonunion firms have higher no-lost-time and lower lost-time claims rates. Unionized firms may encourage occupational injury reporting and reduce risks through training and hazard identification and control strategies.

Nuclear factor kappaB downregulates the transient outward potassium current I(to,f) through control of KChIP2 expression.

RATIONALE: The fast transient outward K(+) current (I(to,f)) plays a critical role in early repolarization of the heart. I(to,f) is consistently downregulated in cardiac disease. Despite its importance, the regulation of I(to,f) in disease remains poorly understood. OBJECTIVE: Because the transcription factor nuclear factor (NF)-κB is activated in cardiac hypertrophy and disease, we studied the role of NF-κB in mediating I(to,f) reductions induced by hypertrophy. METHODS AND RESULTS: Culturing neonatal rat ventricular myocytes in the presence of phenylephrine (PE) plus propranolol (Pro), to selectively activate α(1)-adrenergic receptors, caused reductions in I(to,f), as well as KChIP2 and Kv4.3 expression, while increasing Kv4.2 expression. Inhibition of NF-κB, via overexpression of a phosphorylation-deficient mutant of IκBα (IκBαSA) prevented PE/Pro-induced reductions in I(to,f) and KChIP2 mRNA, without affecting Kv4.2 or Kv4.3 expression, suggesting NF-κB mediates the I(to,f) reductions by repressing KChIP2. Indeed, overexpression of the NF-κB activator IκB kinase-ß also decreased KChIP2 expression and I(to,f) (despite increasing Kv4.2), whereas IκBαSA overexpression elevated KChIP2 and decreased Kv4.2 levels. In addition, the classic NF-κB activator tumor necrosis factor α also induced NF-κB-dependent reductions of KChIP2 and I(to,f). Finally, inhibition of calcineurin did not prevent PE/Pro-induced reductions in KChIP2. CONCLUSIONS: NF-κB regulates KChIP2 and Kv4.2 expression. The reductions in I(to,f) observed following α-adrenergic receptor stimulation or tumor necrosis factor α application require NF-κB-dependent decreases in KChIP2 expression.