Publications by authors named "Oksa P"

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.

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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.

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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.

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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.

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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.

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Objectives: The objective was to investigate trends in the incidence of recognized and suspected cases of occupational diseases in Finland from 1975 to 2013, including variations by industry - and describe and recognize factors affecting variations in incidence.

Design: A register study.

Setting: The data consisted of recognized and suspected cases of occupational diseases recorded in the Finnish Registry of Occupational Diseases (FROD) in 1975-2013.

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The lung just like all other organs is affected by age. The lung matures by the age of 20 and age-related changes start around middle age, at 40-50 years. Exhaled nitric oxide (FNO) has been shown to be age, height and gender dependent.

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Background: We assessed the cancer risks of four different Finnish asbestos-exposed cohorts. We also explored if the cohorts with varying profiles of asbestos exposure exhibited varying relative risks of cancer.

Methods: The incident cancer cases for the asbestos-exposed worker cohorts were updated to the end of 2012 using the files of the Finnish Cancer Registry.

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YKL-40 is a chitinase-like glycoprotein produced by alternatively activated macrophages that are associated with wound healing and fibrosis. Asbestosis is a chronic asbestos-induced lung disease, in which injury of epithelial cells and activation of alveolar macrophages lead to enhanced collagen production and fibrosis. We studied if YKL-40 is related to inflammation, fibrosis, and/or lung function in subjects exposed to asbestosis.

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Background: There is inadequate evidence for the carcinogenicity of cobalt and cobalt compounds in humans. Consequently, the International Agency for Research on Cancer (IARC) has evaluated cobalt metal without tungsten carbide as possibly carcinogenic to humans (Group 2B). The aim of the study was to assess the risk of cancer among workers employed in a Finnish cobalt plant since the beginning of production in 1968.

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Objective: To assess whether cumulative dust exposure in foundry work is associated with airway inflammation measured by the analysis of fractionated exhaled nitric oxide (NO) concentration, or by inflammatory markers in exhaled breath condensate or serum.

Methods: We examined 476 dust-exposed and nonexposed foundry workers, and assessed the individual cumulative exposure to dusts and respirable quartz. Bronchial and alveolar NO production and inflammatory markers in exhaled breath condensate and in serum samples were also analyzed.

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Objectives: To study associations between chest HRCT signs and subsequent deaths in long-term follow-up.

Methods: Lung and pleural signs of 633 asbestos exposed workers (age 45-86, mean 65) screened with HRCT were recorded by using the International Classification of Occupational and Environmental Respiratory Diseases (ICOERD) system, which contains detailed instructions for use and reference images. Subsequent mortality was checked from the national register.

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This field study evaluated the level of muscular, cardiorespiratory and thermal strain of mast and pole workers. We measured the muscular strain using electromyography (EMG), expressed as a percentage in relation to maximal EMG activity (%MEMG). Oxygen consumption (VO2) was indirectly estimated from HR measured during work and expressed as a percentage of maximum VO2 (%VO2max).

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Background: The imbalance between proteases and antiproteases has been proposed to participate to the pathogenesis of chronic obstructive pulmonary disease (COPD) and emphysema. Gene level variation in different metalloproteinases, metalloproteinase inhibitors, and cytokines affecting them may contribute to this imbalance and destruction of the lung parenchyma. We investigated whether polymorphisms in selected protease-antiprotease balance pathway genes predispose to different emphysema subtypes (centrilobular, paraseptal, panlobular, and bullae) and airflow limitation among Finnish construction workers.

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Objectives: Asbestos-exposure causes an inflammatory response driven by alveolar macrophages that can lead to pulmonary fibrosis. In addition to classical inflammatory cytokines, macrophages produce adipokines which regulate the inflammatory response. We studied if adipokines are related to the degree of parenchymal fibrosis, impaired lung function and inflammation in asbestos-exposed subjects.

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The prognosis of lung cancer is poor due to late diagnosis, the lack of established screening programs, and the paucity of early biomarkers for high-risk populations. Plasma proteome analysis was used to identify novel biomarkers for diagnosing lung cancer, and to unravel the mechanisms of underlying pathogenesis. Plasma proteins obtained from asbestos-exposed lung cancer cases detected by CT screening, asbestos-exposed subjects, clinical lung cancer patients, and healthy tobacco smokers, 5-6 cases in each group, were separated by two-dimensional gel electrophoresis, and identified with tandem mass spectrometry (LC-MS/MS).

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Lungs exposed to occupational dust may be especially vulnerable to fatal infections. We followed up asbestos-exposed workers (n=590) originally screened for lung cancer with computed tomography and scored for pleuropulmonary fibrosis. We checked these workers' influenza and pneumonia mortality data (ICD-10 codes J10-J18) in the national register.

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Occupational diseases have been registered since 1964 in Finland. The annual number of suspected or recognized occupational asthma cases is currently approximately 600. Allergy to cow epithelium as the cause of occupational asthma has decreased since the 1980's.

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Background: SERPINE2 (serpin peptidase inhibitor, clade E, member 2) has previously been identified as a positional candidate gene for chronic obstructive pulmonary disease (COPD) and has subsequently been associated to COPD and emphysema in several populations. We aimed to further examine the role of SERPINE2 polymorphisms in the development of pulmonary emphysema and different emphysema subtypes.

Methods: Four single nucleotide polymorphisms (SNPs) in SERPINE2 were analyzed from 951 clinically and radiologically examined Finnish construction workers.

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Background: Exposure to silica dust may cause inflammatory responses, primarily in the lungs, although systemic effects have also been reported. Alveolar inflammation can be demonstrated by increased alveolar concentration of nitric oxide (NO), but information on the effects of silica dust on exhaled NO is sparse. Inflammatory mediators including cytokines are known to take part in silica-induced processes, but the role of adipokines has not been studied previously.

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Background: Pulmonary emphysema is a smoking-induced condition of the lung. Genetically determined differences in the activities of enzymes that metabolize oxidative agents are suspected to modify individual susceptibility to emphysema, as well as other smoking-related pulmonary disorders.

Objectives: We investigated whether polymorphisms in selected xenobiotic-metabolizing enzyme genes predispose to emphysematous changes and airflow limitation among Finnish Caucasian construction workers.

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