Effects of occupational exposure to metal fume PM <sub>2.5</sub> on lung function and biomarkers among shipyard workers: a 3-year prospective cohort study

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Abstract

Objective

This study investigates the associations of α1-antitrypsin, inter-α-trypsin inhibitor heavy chain (ITIH4), and 8-isoprostane with lung function in shipyard workers exposed to occupational metal fume fine particulate matter (PM _2.5), which is known to be associated with adverse respiratory outcomes.

Methods

A 3-year follow-up study was conducted on 180 shipyard workers with 262 measurements. Personal exposure to welding fume PM _2.5 was collected for an 8-h working day. Pre-exposure, post-exposure, and delta (∆) levels of α1-antitrypsin, ITIH4, and 8-isoprostane were determined in urine using enzyme-linked immunosorbent assays. Post-exposure urinary metals were sampled at the beginning of the next working day and analyzed by inductively coupled plasma-mass spectrometry. Lung function measurements were also conducted the next working day for post-exposure.

Results

An IQR increase in PM _2.5 was associated with decreases of 2.157% in FEV ₁, 2.806% in PEF, 4.328% in FEF _25%, 5.047% in FEF _50%, and 7.205% in FEF _75%. An IQR increase in PM _2.5 led to increases of 42.155 µg/g in ∆α1-antitrypsin and 16.273 µg/g in ∆ITIH4. Notably, IQR increases in various urinary metals were associated with increases in specific biomarkers, such as post-urinary α1-antitrypsin and ITIH4. Moreover, increases in ∆ α1-antitrypsin and ∆ITIH4 were associated with decreases in FEV ₁/FVC by 0.008% and 0.020%, respectively, and an increase in ∆8-isoprostane resulted in a 1.538% decline in FVC.

Conclusion

Our study suggests that urinary α1-antitrypsin and ITIH4 could indicate early lung function decline in shipyard workers exposed to metal fume PM _2.5, underscoring the need for better safety and health monitoring to reduce respiratory risks.

Graphical abstract

Supplementary Information

The online version contains supplementary material available at 10.1007/s00420-024-02055-1.

Related collections

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Air pollution has been considered a hazard to human health. In the past decades, many studies highlighted the role of ambient airborne particulate matter (PM) as an important environmental pollutant for many different cardiopulmonary diseases and lung cancer. Numerous epidemiological studies in the past 30 years found a strong exposure-response relationship between PM for short-term effects (premature mortality, hospital admissions) and long-term or cumulative health effects (morbidity, lung cancer, cardiovascular and cardiopulmonary diseases, etc). Current research on airborne particle-induced health effects investigates the critical characteristics of particulate matter that determine their biological effects. Several independent groups of investigators have shown that the size of the airborne particles and their surface area determine the potential to elicit inflammatory injury, oxidative damage, and other biological effects. These effects are stronger for fine and ultrafine particles because they can penetrate deeper into the airways of the respiratory tract and can reach the alveoli in which 50% are retained in the lung parenchyma. Composition of the PM varies greatly and depends on many factors. The major components of PM are transition metals, ions (sulfate, nitrate), organic compound, quinoid stable radicals of carbonaceous material, minerals, reactive gases, and materials of biologic origin. Results from toxicological research have shown that PM have several mechanisms of adverse cellular effects, such as cytotoxicity through oxidative stress mechanisms, oxygen-free radical-generating activity, DNA oxidative damage, mutagenicity, and stimulation of proinflammatory factors. In this review, the results of the most recent epidemiological and toxicological studies are summarized. In general, the evaluation of most of these studies shows that the smaller the size of PM the higher the toxicity through mechanisms of oxidative stress and inflammation. Some studies showed that the extractable organic compounds (a variety of chemicals with mutagenic and cytotoxic properties) contribute to various mechanisms of cytotoxicity; in addition, the water-soluble faction (mainly transition metals with redox potential) play an important role in the initiation of oxidative DNA damage and membrane lipid peroxidation. Associations between chemical compositions and particle toxicity tend to be stronger for the fine and ultrafine PM size fractions. Vehicular exhaust particles are found to be most responsible for small-sized airborne PM air pollution in urban areas. With these aspects in mind, future research should aim at establishing a cleared picture of the cytotoxic and carcinogenic mechanisms of PM in the lungs, as well as mechanisms of formation during internal engine combustion processes and other sources of airborne fine particles of air pollution.

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Is Open Access

Lung function decline in COPD

Claudio Tantucci, Denise Modina (2012)

The landmark study of Fletcher and Peto on the natural history of tobacco smoke-related chronic airflow obstruction suggested that decline in the forced expiratory volume in the first second (FEV1) in chronic obstructive pulmonary disease (COPD) is slow at the beginning, becoming faster with more advanced disease. The present authors reviewed spirometric data of COPD patients included in the placebo arms of recent clinical trials to assess the lung function decline of each stage, defined according to the severity of airflow obstruction as proposed by the Global Initiative for Chronic Obstructive Lung Disease (GOLD) guidelines. In large COPD populations the mean rate of FEV1 decline in GOLD stages II and III is between 47 and 79 mL/year and 56 and 59 mL/year, respectively, and lower than 35 mL/year in GOLD stage IV. Few data on FEV1 decline are available for GOLD stage I. Hence, the loss of lung function, assessed as expiratory airflow reduction, seems more accelerated and therefore more relevant in the initial phases of COPD. To have an impact on the natural history of COPD, it is logical to look at the effects of treatment in the earlier stages.

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Author and article information

Contributors

Hsiao-Chi Chuang:

ORCID: http://orcid.org/0000-0003-4651-5192

chuanghc@tmu.edu.tw

Journal

Journal ID (nlm-ta): Int Arch Occup Environ Health

Journal ID (iso-abbrev): Int Arch Occup Environ Health

Title: International Archives of Occupational and Environmental Health

Publisher: Springer Berlin Heidelberg (Berlin/Heidelberg )

ISSN (Print): 0340-0131

ISSN (Electronic): 1432-1246

Publication date (Electronic): 13 March 2024

Publication date PMC-release: 13 March 2024

Publication date (Print): 2024

Volume: 97

Issue: 4

Pages: 401-412

Affiliations

[1 ]Program in Global Health and Health Security, College of Public Health, Taipei Medical University, ( https://ror.org/05031qk94) Taipei, Taiwan

[2 ]Faculty of Public Health, Da Nang University of Medical Technology and Pharmacy, ( https://ror.org/03ecpp171) Da Nang, Vietnam

[3 ]School of Public Health, National Defense Medical Center, ( https://ror.org/02bn97g32) Taipei, Taiwan

[4 ]Division of Family Medicine, Department of Family and Community Medicine, Tri-Service General Hospital, ( https://ror.org/007h4qe29) Taipei, Taiwan

[5 ]Division of Geriatric Medicine, Department of Family and Community Medicine, Tri-Service General Hospital, ( https://ror.org/007h4qe29) Taipei, Taiwan

[6 ]School of Medicine, National Defense Medical Center, ( https://ror.org/02bn97g32) Taipei, Taiwan

[7 ]GRID grid.482591.3, Institute of Labor, Occupational Safety and Health, Ministry of Labor, ; New Taipei City, Taiwan

[8 ]School of Public Health, College of Public Health, Taipei Medical University, ( https://ror.org/05031qk94) Taipei, Taiwan

[9 ]Department of Public Health, School of Medicine, College of Medicine, Taipei Medical University, ( https://ror.org/05031qk94) Taipei, Taiwan

[10 ]Division of Pulmonary Medicine, Department of Internal Medicine, Shuang Ho Hospital, Taipei Medical University, ( https://ror.org/05031qk94) New Taipei City, Taiwan

[11 ]Inhalation Toxicology Research Lab (ITRL), School of Respiratory Therapy, College of Medicine, Taipei Medical University, ( https://ror.org/05031qk94) 250 Wuxing Street, Taipei, 11031 Taiwan

[12 ]GRID grid.412896.0, ISNI 0000 0000 9337 0481, Cell Physiology and Molecular Image Research Center, Wan Fang Hospital, , Taipei Medical University, ; Taipei, Taiwan

Author information

Hsiao-Chi Chuang http://orcid.org/0000-0003-4651-5192

Article

Publisher ID: 2055

DOI: 10.1007/s00420-024-02055-1

PMC ID: 10999385

PubMed ID: 38480609

SO-VID: cef60a0f-548a-4863-846c-e59f265e2d51

License:

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/.

History

Date received : 8 December 2023

Date accepted : 5 February 2024

Funding

Funded by: FundRef http://dx.doi.org/10.13039/501100004663, Ministry of Science and Technology, Taiwan;

Award ID: 110-2314-B-016-009

Award ID: 111-2314-B-038-079

Award ID: 107-2314-B-016 -045 -MY3

Award ID: 112-2628-B-038-010-MY3

Award Recipient : Ching-Huang Lai

Funded by: Minstry of Defense

Award ID: MND-MAB-110-138

Custom metadata

ScienceOpen disciplines: Occupational & Environmental medicine

Keywords: α1-antitrypsin,itih4,lung function,oxidative stress,particulate matter,welding

Data availability:

ScienceOpen disciplines: Occupational & Environmental medicine

Keywords: α1-antitrypsin, itih4, lung function, oxidative stress, particulate matter, welding