lung diseases, cardiovascular diseases, and other age-related chronic conditions—is an age-associated immune deregulation charac- terized by high blood levels of pro-inflam- matory mediators (Ferrucci & Fabbri, 2018; Kovacs et al., 2017). Inflammaging refers to a skewing toward systemic inflammation, which is paradoxically couplved with a sup- pressed ability to respond to immunological threats (Franceschi et al., 2000). In addition, age-related changes in the lung’s innate and adaptive immune response are linked to poor prognosis, recovery, and increased suscep- tibility to environmental exposure-induced injury (Cho & Stout-Delgado, 2020). Aging and Lung Physiology The major changes associated with aging are reduced lung elasticity, respiratory muscle strength, and chest wall compliance, all of which can be influenced by impaired lung growth in early childhood and adolescence. Lung function declines with age but forced vital capacity (FVC) begins to decline later than forced expiratory volume (FEV) and at a slower rate (Dyer, 2012). This pattern results in a natural fall in the FEV/FVC ratio, which can result in overdiagnosis of COPD and hence the need to ensure FEV is <80% before confirming the diagnosis. As older adults probably have a diminished response to hypoxia and hypercapnia, they become more vulnerable to ventilator failure during high-demand states such as heart failure and pneumonia and, therefore, to possible poor outcomes (Dyer, 2012). Lung function starts to decline at 35 years of age, and aging is associated with increased functional resid- ual capacity; reduced expiratory volume; reduced FVC and FEV1 by 30 ml/year and 20 ml/year, respectively; reduced diusion capacity for carbon dioxide; and lower rest- ing arterial oxygen (Cho & Stout-Delgado, 2020). This decline indicates that older age is an additional challenge to individuals who had occupational exposures.
FIGURE 3
Deaths by Age of Residents in the United States, 2005–2014 12,000
10,000
8,000
6.000
4,000
2,000
0
Age (Years) 15–24 25–34 35–44 45–54 55–64 65–74 75–84
≥85
Coal Workers' Pneumoconiosis and Related Exposure Byssinosis and Related Exposure Malignant Mesothelioma
Asbestosis and Related Exposure Silicosis and Related Exposure All Pneumoconiosis and Related Exposure Hypersensitivity Pneumonitis
TABLE 2
Mortality and Deaths in the United States From Work-Related Respiratory Diseases
Age (Years)
Mortality (#)
Deaths From Work-Related Respiratory Diseases (#)
2019
2020
1995–2004
2005–2014
15–24 25–34 35–44 45–54 55–64 65–74 75–84
29,771 59,178 82,986 160,393 374,937 555,559 688,027 873,746
35,816 73,486 104,490 191,142 440,549 674,507 822,084
30
46
106 464
167 494
1,742 6,043
1,941 6,397
17,926 29,718 14,406
15,533 26,576 16,681
≥85
1,012,805
Major Occupational Lung Diseases
with age represents a critical failure because this type of immunity plays a key role in pro- tecting the lung’s mucosal surface from air- borne pathogens. Although the aging innate immune system augments the release of pro- inflammatory cytokines, thus contributing to inflammation, it is simultaneously handi-
capped in its ability to recognize pathogens, signal through toll-like receptor (TLR) cas- cades, present antigens, undergo chemotaxis, and phagocytose foreign material (Shaw et al., 2013). Furthermore, inflammaging—which is implicated in the pathogenesis of chronic
Asbestosis Asbestosis is a chronic interstitial lung con- dition caused by prolonged exposure to high concentrations of asbestos fibers (American Lung Association, 2024; Bhandari et al., 2022). The latency period for asbestosis,
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October 2024 • Journal of Environmental Health
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