The prevalence of respiratory symptoms and diseases and declined lung function among foundry workers.

Background: Foundry workers are occupationally exposed to a variety of inhalable chemical substances. Occupational exposure to vapors, gases, dusts, and fumes can lead to adverse health effects on the respiratory system and cause chronic respiratory diseases, such as interstitial lung diseases (ILDs), chronic obstructive lung disease (COPD), chronic bronchitis, and emphysema. Research on respiratory symptoms, diseases, and lung function in foundry workers over the past few decades has been limited.

An Increase in Plasma Adipsin Levels Is Associated With Higher Cumulative Dust Exposure and Airway Obstruction in Foundry Workers.

Objective: The aim of the study was to assess whether plasma adipokine levels (adipsin, adiponectin, leptin, and resistin) are associated with pulmonary function in foundry workers.

Methods: We examined 65 dust-exposed foundry workers and 40 nonexposed controls and analyzed their lung function and plasma adipokine levels at baseline and after approximately 7 years of follow-up.

Results: A higher increase in plasma adipsin was associated with the development of airway obstruction in exposed subjects during follow-up after adjusting for body mass index changes during the follow-up period.

High alveolar nitric oxide is associated with steeper lung function decline in foundry workers.

Occupational dust exposure induces inflammatory responses that often precede the onset of clinical disease. Inflammation in the peripheral part of the lung can be demonstrated by measuring the alveolar NO concentration (CNO) in exhaled breath. The aim of the study was to assess whether cumulative dust exposure affects the change in CNO during follow-up and whether baseline CNO can predict an impairment in lung function during follow-up in foundry workers.

Effects of occupational cobalt exposure on the heart in the production of cobalt and cobalt compounds: a 6-year follow-up.

Objective: It has been suspected that cobalt is toxic to the heart. It can cause cardiotoxicity in heavily exposed humans and in experimental systems. The issue of interest for this study is whether cobalt also affects the myocardium at occupational exposure levels.

Loss of Cln5 leads to altered Gad1 expression and deficits in interneuron development in mice.

The Finnish-variant late infantile neuronal ceroid lipofuscinosis, also known as CLN5 disease, is caused by mutations in the CLN5 gene. Cln5 is strongly expressed in the developing brain and expression continues into adulthood. CLN5, a protein of unknown function, is implicated in neurodevelopment but detailed investigation is lacking.