Anette Kocbach Bølling

Environmental noise is the second largest environmental risk factor in disease burden estimates for Europe. While socioeconomic inequalities in noise exposure have been reported, the impact of socioeconomic status (SES) on the disease burden attributable to noise exposure has to our knowledge not been reported previously. The aim of this study is to assess the impact of SES on traffic noise exposure and the associated disease burden in selected Nordic populations. We employed nationwide data on road traffic noise exposure and SES from Danish and Norwegian Nationwide Models. The impact of household income and education on traffic noise exposure was assessed using linear regression analyses. Burden of disease estimates were calculated for populations stratified according to their level of income and education in terms of Disability-Adjusted Life Years (DALY) for high degree of noise annoyance, high degree of sleep disturbance and ischaemic heart disease. The most consistent finding observed for the Danish population was that, compared to medium and low household income, high household income was associated with lower noise exposure. Moreover, the burden of disease estimates for high noise annoyance were up to 20% lower in the high compared to the lower household income groups.

The Tobacco Products Directive (TPD) defines enhanced reporting obligations applying to 15 priority additives added to cigarettes and roll-your-own tobacco. A consortium of 12 international tobacco companies submitted 14 reports that were reviewed by an independent scientific body within the...

The European Union Tobacco Products Directive (EU TPD) mandates enhanced reporting obligations for tobacco manufacturers regarding 15 priority additives. Within the Joint Action on Tobacco Control (JATC), a review panel of independent experts was appointed for the scientific evaluation of the...

Bisphenol A (BPA) and phthalates are common environmental contaminants that have been proposed to influence incidence and development of types 1 and 2 diabetes. Thus, effects of BPA and three phthalate metabolites (monoisobutyl phthalate (MiBP), mono-n-butyl phthalate (MnBP), and mono-(2-ethylhexyl) phthalate (MEHP)) were studied in the pancreatic β-cell line INS-1E, after 2–72 h of exposure to 5–500 μM. Three endpoints relevant to accelerated development of types 1 or 2 diabetes were investigated: β-cell viability, glucose-induced insulin secretion, and β-cell susceptibility to cytokine-induced cell death. BPA and the phthalate metabolites reduced cellular viability after 72 h of exposure, with BPA as the most potent chemical. Moreover, BPA, MEHP, and MnBP increased insulin secretion after 2 h of simultaneous exposure to chemicals and glucose, with potency BPA > MEHP > MnBP. Longer chemical exposures (24–72 h) showed no consistent effects on glucose-induced insulin secretion, and none of the environmental chemicals affected susceptibility to cytokine-induced cell death. Overall, BPA was more potent than the investigated phthalate metabolites in affecting insulin secretion and viability in the INS-1E pancreatic β-cells. In contrast to recent literature, concentrations with relevance to human exposures (1–500 nM) did not affect the investigated endpoints, suggesting that this experimental model displayed relatively low sensitivity to environmental chemical exposure.