The extent of injury depends on the dust particle implicated through inflammation and fibrosis; however, some dust particles are biologically inert, giving rise to no clini- cal outcome (Akgün, 2018; Barber & Fish- wick, 2020; Cullinan & Reid, 2013; DeLight & Sachs, 2023). In addition, individual susceptibility, PPE use, age, and smoking status are associated with pneumoconiosis (Akgün, 2018). Common pneumoconioses are fibrotic, caused by inhaling particles such as silica, asbestos fibers, beryllium, talc, and coal dust (Barber & Fishwick, 2020; DeLight & Sachs, 2023). There is no cure for pneumo- coniosis, leaving protection from exposure the best way to prevent the disease (DeLight & Sachs, 2023). Treatment options for pneumoconiosis are limited; lung transplant is the only life-saving therapeutic option for end-stage pneumoconiosis (Qi et al., 2021). Pneumoconiosis has a long latency period, following many years of exposure to dust particles and fiber (Barber & Fishwick, 2020). Pneumoconiosis can lead to seri- ous complications depending on the dust, with the most serious complication being fibrosis and pleuropulmonary malignancy (DeLight & Sachs, 2023). Per the Interna- tional Labour Organization (ILO) definition, pneumoconiosis requires dust accumulation for its development and should be dier- entiated from other dust-related lung dis- eases such as asthma, byssinosis, berylliosis, COPD, and hypersensitivity pneumonitis, as their development is independent of dust accumulation (Akgün, 2018). The diagnosis of pneumoconiosis relies mainly on a history of exposure and chest radiography. The ILO International Classifica- tion of Radiographs of Pneumoconioses, created in 2011 and revised in 2022 with the intro- duction of digitally acquired radiographic standard images, provided the criteria for the diagnosis of pneumoconiosis, because high- resolution computed tomography (HRCT) is more sensitive to early detection than chest radiography and thus is considered a more useful screening tool for pneumoconiosis (Qi et al., 2021). Malignant Mesothelioma Malignant mesothelioma is a rare and aggres- sive cancer that results from asbestos expo- sure (Jain & Wallen, 2023; Moore et al.,
2008; Pouliquen & Kopecka, 2021). Even though mesothelioma can occur in the peri- cardium, peritoneum, or tunica vaginalis (tes- tes), it predominantly occurs in the pleura of the lungs (Jain & Wallen, 2023; Kao et al., 2010; Moore et al., 2008; National Center for Chronic Disease Prevention, 2022). Malig- nant mesothelioma has a long latency period of 20–30 years following asbestos exposure to disease onset (Cugliari et al., 2020). Diagnosis of malignant mesothelioma depends mainly on histological findings from biopsy and clinical, radiological, and surgi- cal findings, including a history of asbestos exposure (Husain et al., 2018). Radiological imaging such as X-ray, CT, magnetic reso- nance imaging (MRI), and positron emission tomography (PET) are used to diagnose and stage malignant mesothelioma (Jain & Wal- len, 2023; Moore et al., 2008). The three histological subtypes of mesothelioma cells are epithelioid, sarcomatoid, and biphasic (mixed), with epithelioid having the better outcome (Husain et al., 2018; Jain & Wal- len, 2023). Chemotherapy and radiotherapy are used with limited clinical eect; how- ever, treatment for malignant mesothelioma depends on tumor staging and the potential for surgical resection (Jain & Wallen, 2023; Kao et al., 2010). Hypersensitivity Pneumonitis Hypersensitivity pneumonitis (HP) is an immune-mediated interstitial lung disease in susceptible or sensitized individuals that results from the inhalation of antigens found in the environment (Barnes et al., 2022; Churg, 2022; Costabel et al., 2020; Hamb- lin et al., 2022; Raghu et al., 2020). These antigens can come from bacteria, mycobac- teria, fungi, animal protein, plant protein, enzymes, chemicals, and metals (Costabel et al., 2020). Subsets of HP and associated occu- pational exposure include farmer’s lung, bird or pigeon fancier’s lung, hot tub lung, cheese worker’s lung, bagassosis (from a fibrous cane-sugar residue), mushroom worker’s lung, and malt worker’s lung (Chandra & Cherian, 2023; Costabel et al., 2020). The source of antigen varies depending on the activity involved, including occupational exposure with bird-related (fancier lungs), bacteria-related (farmer’s lung), and fungal- related (humidifier lung/summer-type lung) antigens being the most common (Costabel
et al., 2020). Classifications of HP include acute, subacute, and chronic schemes (Chan- dra & Cherian, 2023; Churg, 2022; Leone & Richeldi, 2020; Raghu et al., 2020) and the proposed acute, chronic-nonfibrotic, and chronic-fibrotic schemes (Churg, 2022; Cos- tabel et al., 2020). Symptoms of HP include dyspnea, cough, and mid-inspiratory squeaks. Patients can experience weight loss, flu-like symptoms, chest tightness, wheezing, rales, and cya- nosis on physical exam (Leone & Richeldi, 2020; Raghu et al., 2020). Diagnosing HP can be challenging and dierentiating between fibrotic HP and other interstitial fibrotic lung diseases poses therapeutic challenges, underscoring the need for accurate diagnosis (Churg, 2022; Costabel et al., 2020). Removing the causative agent from the work environment is critical to the poten- tial reversal of mild cases, while the pres- ence of pulmonary fibrosis signals a poor prognosis with a median survival of 3–5 years. Furthermore, age and other factors have been associated with worse outcomes (Chandra & Cherian, 2023). History of work-related exposure is crucial in diagnos- ing HP; global spirometry, diusing capacity for carbon monoxide (DLCO), and forced vital capacity (FVC) are used as predictive factors in patient survival. FVC, however, can be insensitive in the presence of fibro- sis (Hamblin et al., 2022; Leone & Richeldi, 2020). Additionally, HRCT (which has a high sensitivity), bronchioalveolar lavage, and surgical biopsy for histology are com- monly used for diagnosing HP. Diagnosis is controversial because there is no consensus standard for HP diagnosis due to its overlap with other interstitial lung diseases (Barnes et al., 2022; Hamblin et al., 2022; Leone & Richeldi, 2020). Work-Related Asthma Asthma is a chronic and noncommunicable disease of the air passages characterized by inflammation and narrowing of the lower airways (Hashmi & Cataletto, 2024; Laditka et al., 2020; Mims, 2015). This inflammation leads to an associated increase in existing bronchial hyperresponsiveness to a variety of stimuli (Hashmi & Cataletto, 2024; Mims, 2015). Work-related asthma has two classifi- cations: occupational asthma (OA) caused by exposure at the workplace, and work-exacer-
17
November 2024 • Journal of Environmental Health
Powered by FlippingBook