Occupational and environmental exposure can directly cause specific lung diseases, and can also induce autoimmune diseases that can lead to various types of interstitial lung diseases. In recent years, it was discovered that certain occupational and environmental exposure was related to the increased risk of Idiopathic pulmonary fibrosis (IPF) disease and progression, including metal and mineral dust, wood dust, organic dust, asbestos dust, silica dust, cigarette smoke and air pollution. IPF is a chronic progressive fibrotic lung disease of unknown etiology, with a characteristic imaging and histologic pattern called usual interstitial pneumonia. This article is a review based on the correlation and mechanism of occupational and environmental exposure in the pathogenesis and disease progression of IPF to improve the understanding of the disease and promote the formulation of treatment plans.
Humans ; Idiopathic Pulmonary Fibrosis/etiology* ; Dust ; Environmental Exposure/adverse effects* ; Occupational Exposure/adverse effects* ; Lung Diseases, Interstitial

After one-month of oral treatment with traditional Chinese medicine decoction, without using other drugs, the lung inflammatory exudate, pulmonary fibrosis and quality of life of a 61-year-old female patient with corona virus disease 2019 (COVID-19) were significantly improved. No recurrence or deterioration of the patient's condition was found within seven weeks of treatment and follow-up, and no adverse events occurred, indicating that oral Chinese medicine decoction was able to improve the pulmonary inflammation and fibrosis in a patient recovering from COVID-19, but further research is still needed.
Administration, Oral ; COVID-19/virology* ; Drugs, Chinese Herbal/therapeutic use* ; Exudates and Transudates ; Female ; Humans ; Inflammation/etiology* ; Lung/pathology* ; Magnoliopsida ; Medicine, Chinese Traditional ; Middle Aged ; Phytotherapy ; Pulmonary Fibrosis/etiology* ; SARS-CoV-2

OBJECTIVETo evaluate the characteristics of the serious complications of 17 cases with measles in ICU.

METHODSeventeen cases with measles with serious complications in ICU in Anhui Provincial Children's Hospital were recruited from May 2012 to May 2013. Clinical characteristics, image finding, and prognosis were analyzed retrospectively. IgM antibody was positive in all the 17 cases, which included 9 male cases, 8 female cases, and their age was from 2 months to 10 years.

RESULTAll the 17 patients received mechanical ventilation because of severe respiratory distress within 1 week of onset, of which 14 cases were complicated with acute respiratory distress syndrome (acute ARDS), 6 cases of tension pneumothorax, 3 cases were complicated with bronchitis, laryngeal obstruction III degrees, and totally 7 cases died. The survived 10 patients were followed up for 1 year, 1 patient with localized pneumothorax, bronchopleural fistula, 1 case of mild pulmonary fibrosis, 1 case of acute laryngitis with persistent hoarseness, and mild inspiratory dyspnea were found. The remaining 7 cases fully recovered. Fourteen cases failed to inoculate measles vaccine.

CONCLUSIONA higher risk of death and poor prognosis were found in children with measles who needed to be treated in PICU, especially for ARDS with pneumothorax. Laryngitis needed long time to cure and had weaning difficulties, and the case associated with pleural effusion or bronchopleural fistula must be treated with surgery, and the patients easily develop secondary bacterial infection.

Child ; Dyspnea ; Female ; Humans ; Intensive Care Units, Pediatric ; Lung Diseases ; etiology ; Male ; Measles ; complications ; Pleural Effusion ; Prognosis ; Pulmonary Fibrosis ; Respiration, Artificial ; Retrospective Studies

BACKGROUNDCombined emphysema and pulmonary fibrosis, including idiopathic pulmonary fibrosis (IPF), is a distinct disorder described with upper-lobe emphysema and lower-lobe fibrosis on chest computed tomography. Smoking appears to be the predominant risk factor for this disorder. We aimed to compare clinical features, smoking history, physiological and radiological findings between IPF with and without emphysema.

METHODSA sample of 125 IPF patients over a period of 48 months were evaluated. High resolution CT scans were reviewed blinded to clinical data. The IPF patients with or without emphysema were classified accordingly.

RESULTSThe prevalence of emphysema in this IPF sample was 70/125. IPF with emphysema was significantly associated with smoking status (OR 63; 95% CI 4.4 to 915; P = 0.002) and smoking pack year (OR 1.1; 95% CI 1.05 to 1.13; P = 0.000). The patients with IPF and emphysema had a higher decrease in carbon monoxide diffusing capacity adjusted for alveolar volume ((58±19)% pred vs. (66±21)% pred; P = 0.021) and a higher prevalence of pulmonary hypertension (24/70 vs. 7/55; P = 0.006). The two groups of patients had similar forced and residual volumes. No significant differences were found in cell differentials of bronchoalveolar lavage or the scores of fibrosis on chest CT. Survival of the patients with emphysema was significantly less than that of patients with IPF alone.

CONCLUSIONSCigarette smoking induces IPF combined with emphysema. Emphysema further impairs physiological function and increases the prevalence of pulmonary hypertension that leads to poor prognosis. The inclusion of the patients with combined pulmonary fibrosis and emphysema in IPF clinical trials may lead to under evaluation of the effect of treatment in patients.

Aged ; Female ; Humans ; Idiopathic Pulmonary Fibrosis ; etiology ; physiopathology ; Male ; Middle Aged ; Pulmonary Emphysema ; complications ; physiopathology ; Smoking ; adverse effects

BACKGROUNDGiant cell interstitial pneumonia (GIP) was a rare form of pneumoconiosis, associated with exposure to hard metals, which had been reported mostly as isolated case reports. We described eight cases of GIP diagnosed in our hospital during the past seven years, with particular reference to new findings.

METHODSEight patients with GIP confirmed by biopsy in the Nanjing Drum Tower Hospital affiliated to Medical School of Nanjing University from 2005 to 2011 were retrospectively analyzed. For each patient, the occupy histories and medical records were thoroughly reviewed and clinic data were extracted. Two radiologists, without knowledge of any of the clinical and functional findings, independently reviewed the HRCT scans of all patients. Follow-up data were collected.

RESULTSAmong the eight patients, seven had a history of exposure to hard metal dusts, one denied an exposure history. The most common manifestations were cough and dyspnea. One patient initiated with pneumothorax and another pleural effusion, both of which were uncommon to GIP. The main pathologic appearances were the presence of macrophages and multinucleated giant cells in the alveolar space. The clinical symptoms and radiographic abnormalities were obviously improved after cessation of exposure and receiving corticosteroid treatments, recurrences were observed in two patients when they resumed work. In spite of exposure cessation and corticosteroid treatment, one patient developed pulmonary fibrosis at seven years follow-up.

CONCLUSIONSAwareness of the patients' occupational history often provided clues to the diagnosis of GIP. Histopathologic examinations were necessary to establish the right diagnosis. Exposure cessation was of benefit to most patients; however, pulmonary fibrosis was possible in spite of exposure cessation and corticosteroid treatment. Better ways should be found out to improve the outcome and quality of life.

Adult ; Alloys ; toxicity ; Cobalt ; toxicity ; Female ; Humans ; Lung ; pathology ; Lung Diseases, Interstitial ; diagnosis ; etiology ; Male ; Middle Aged ; Pulmonary Fibrosis ; diagnosis ; etiology ; Retrospective Studies ; Tungsten ; toxicity ; Young Adult

OBJECTIVETo review the studies investigating the increased risk of lung cancer in patients with idiopathic pulmonary fibrosis (IPF).

DATA SOURCESData cited in this review were obtained mainly from PubMed and Medline from 1999 to 2013 and highly regarded older publications were also included.

STUDY SELECTIONWe identified, retrieved and reviewed the information on the frequency, risk factors, anatomical features, histological types, clinical manifestations, computed tomography findings and underlying mechanisms of lung cancer in IPF patients.

RESULTSThe prevalence rates of lung cancer in patients with IPF (4.8% to 48%) are much higher than patients without IPF (2.0% to 6.4%). The risk factors for lung cancer in IPF include smoking, male gender, and age. Lung cancers often occur in the peripheral lung zones where fibrotic changes are predominant. Adenocarcinoma and squamous cell carcinoma are the most common types of lung cancer in patients with IPF. Radiologic features of these patients include peripherally located, ill-defined mass mimicking air-space disease. The underlying mechanisms of the development of lung cancer in patients with IPF have not been fully understood, but may include the inflammatory response, epithelial injury and/or abnormalities, aberrant fibroblast proliferation, epigenetic and genetic changes, reduced cell-to-cell communication, and activation of specific signaling pathways.

CONCLUSIONSThese findings suggest that IPF is associated with increased lung cancer risk. It is necessary to raise the awareness of lung cancer risk in IPF patients among physicians and patients.

Age Factors ; Female ; Humans ; Idiopathic Pulmonary Fibrosis ; complications ; epidemiology ; genetics ; Lung Neoplasms ; epidemiology ; etiology ; genetics ; Male ; Risk Factors ; Sex Factors

Evidence suggests that diabetes mellitus (DM) is associated with idiopathic pulmonary fibrosis (IPF). According to the new IPF guidelines, high-resolution computed tomography (HRCT) is an essential means of diagnosing IPF. We investigated the relationship between IPF and DM in patients treated between 2003 and 2007. Newly diagnosed IPF patients in large university teaching hospitals in Korea were enrolled from January 2003 to December 2007. We retrospectively analyzed 1,685 patients using the interstitial lung disease (ILD) registry. In total, 299 IPF patients (17.8%) also had DM. The mean age of our subjects was 68.0 +/- 9.4 yr. HRCT showed significantly more reticular and honeycomb patterns in IPF patients with DM than in IPF patients without DM (P = 0.014, P = 0.028, respectively). Furthermore, significantly higher incidences of hypertension, cardiovascular diseases, and other malignancies (except lung cancer) were found in IPF patients with DM than in IPF patients without DM. In conclusion, IPF patients with DM are more likely to have the usual interstitial pneumonia (UIP) pattern, including reticular and honeycomb patterns, on HRCT than are those without DM.
Aged ; Cardiovascular Diseases/epidemiology/etiology ; Diabetes Mellitus, Type 2/*complications ; Female ; Humans ; Hypertension/epidemiology/etiology ; Idiopathic Pulmonary Fibrosis/complications/*diagnosis/radiography ; Incidence ; Male ; Middle Aged ; Neoplasms/epidemiology/etiology ; Registries ; Republic of Korea/epidemiology ; Retrospective Studies ; Tomography, X-Ray Computed

This study is to determine the preventive effect and mechanism of targeting IL-17A on pulmonary inflammation and fibrosis after acute lung injury. Mice were treated with anti-IL-17A antibody on the day 7 and sacrificed on the day 14 after bleomycin lung injury. The pulmonary inflammatory status and the deposition of collagen were measured by HE and Sirius stains staining. The contents of hydroxyproline and collagen were measured by using commercial kits. The survival rate of mice was calculated by Kaplan-Meier methods. The inflammatory cytokines in bronchoalveolar lavage fluid were measured by ELISA and the expressions of inflammation-related molecules were detected by Western blotting assay. Targeting of IL-17A could prevent the development of lung inflammation, decrease collagen deposition and the contents of hydroxyproline, and protect against the development of pulmonary fibrosis, which together led to an increase in the animal survival. Moreover, blocking IL-17A decreased the expression ofpro-fibrotic cytokines such as IL-17A, TGF-beta1 and IL-13; increased the expression of anti-fibrotic or anti-inflammatory factors such as IFN-gamma, COX-2, 5-LOX, 15-LOX. Indeed, IL-17A antagonism suppressed the activation of pro-inflammatory p65NF-kappaB but enhanced the activation of pro-resolving p50NF-kappaB. In conclusion, that blockade of IL-17A prevents the development of pulmonary fibrosis from acute lung injury, is because blocking IL-17A may prevent acute inflammation converting to chronic inflammation.
Acute Lung Injury ; chemically induced ; complications ; Animals ; Bleomycin ; Collagen ; metabolism ; Hydroxyproline ; metabolism ; Interleukin-13 ; metabolism ; Interleukin-17 ; antagonists & inhibitors ; metabolism ; Male ; Mice ; Mice, Inbred C57BL ; NF-kappa B p50 Subunit ; metabolism ; Pneumonia ; etiology ; metabolism ; Pulmonary Fibrosis ; etiology ; metabolism ; prevention & control ; Random Allocation ; Transcription Factor RelA ; metabolism ; Transforming Growth Factor beta1 ; metabolism ; Up-Regulation

OBJECTIVETo explore the role of hypoxia-inducible factor 1alpha (HIF-1α) in early lung fibrosis of rats with acute paraquat (PQ) poisoning.

METHODSForty eight healthy SD rats were randomly divided into control group (6 rats) and paraquat poisoning group (42 rats). Control group was exposed to 1 ml normal solution by gastric gavage. The paraquat group was exposed to 1 ml paraquat solution (50 mg/kg) by gastric gavage for 2, 6, 12, 48, 72 and 120 h, respectively. The arterial blood gas analysis (PaO(2)) was detected. The pathological examinations of lung tissues were performed by HE and Mason staining. HIF-1α in lung tissues were measured by immunofluorescence. Western blot assay was used to detect the expression levels of HIF-1α protein in lung tissues.

RESULTSPaO2 of rats exposed to paraquat for 72 h was (62.33 ± 0.22) mm Hg, which was significantly lower than that (96.00 ± 5.20) of control group (P < 0.05). Pathological examination by HE staining indicated that the acute diffuse lesion appeared in the alveolar capillary endothelium, epithelia and interstitial tissues, and there was the inflammatory cell infiltration in the alveolar of rats exposed to paraquat at 2 h after exposure. At 12 h after exposure, the interstitial edema in lung tissues of rats decreased and the alveolar space became narrow. At 120 h after exposure, there were the alveolar structure derangement, abundant cicatrix, more fibroblasts and peripheral inflammation absorption. Pathological examination by Masson staining showed that there was obvious collagen deposition in the alveolar epithelia at 2h after exposure, the increased collagen fibrosis at 24 and 48 h after exposure and the obvious damage of alveolar tissues or much more fibrous connective tissue deposition at 120 h after exposure. The results of western blot and immunofluorescence assays exhibited that the expression levels of HIF-1α in lung tissues at 2, 24 and 48 h after exposure significantly increased, as compared with control group (P < 0.05), but there were no significant differences of HIF-1α expression among sub-groups at different time points after exposure.

CONCLUSIONThe results of present study shown that there were the pulmonary fibrosis and increased expression of HIF-1α in acute PQ poisoning rats at the early stage, and HIF-1α may be associated with pulmonary fibrosis.

Acute Lung Injury ; chemically induced ; complications ; metabolism ; Animals ; Hypoxia-Inducible Factor 1, alpha Subunit ; metabolism ; Male ; Paraquat ; poisoning ; Pulmonary Fibrosis ; etiology ; metabolism ; pathology ; Rats ; Rats, Sprague-Dawley

BACKGROUNDThe condition of concomitant upper lobe emphysema and lower lobe fibrosis as identified by computer tomography is known as combined pulmonary fibrosis and emphysema (CPFE). CPFE has distinct clinical characteristics compared with emphysema alone (EA) and idiopathic pulmonary fibrosis (IPF) without emphysema. However, the pulmonary inflammation characteristics of CPFE are not well known, and the differences between CPFE and the other two diseases with regards to pulmonary inflammation need to be explored. The pulmonary inflammatory characteristics were investigated in CPFE patients and compared with EA and IPF.

METHODSFraction exhaled nitric oxide (Fe,NO) and differential cell counts, the concentrations of monokine induced by interferon gamma (MIG/CXCL9), interferon-inducible protein 10 (IP-10/CXCL10), and interferon-inducible T cell alpha chemoattractant (I-TAC/CXCL11) were measured in induced sputum obtained from subjects with CPFE (n = 22), EA (n = 22), IPF (n = 14), and healthy volunteers (HV, n = 12). In addition, immunohistochemistry was used to quantify the expression of nitric oxide synthases in alveolar macrophages in 23 lung tissues from patients and control subjects.

RESULTSThe CPFE group had higher alveolar NO than subjects in the EA and HV groups (P = 0.009, P = 0.001, respectively) but not than the IPF group (P > 0.05). Numbers of sputum eosinophils were significantly elevated in CPFE and IPF groups compared with the HV group (P = 0.001, P = 0.008). In contrast, eosinophil counts in EA group did not differ from those in the HV group. Compared with the EA and HV groups, the CPFE group had a lower concentration of I-TAC/CXCL11 in sputum supernatants (P = 0.003, P = 0.004). Immunoreactivity for inducible nitric oxide synthase (iNOS) was higher in the CPFE group than in the EA group (P = 0.018, P = 0.006, respectively).

CONCLUSIONSThe pulmonary inflammation of CPFE group is more similar to IPF group, while the distal airway inflammation is more significant in CPFE and IPF groups than in EA group. Lung eosinophil cell infiltration and high NOS expression in alveolar macrophage might participate in this pathogenesis.

Aged ; Breath Tests ; Chemokines ; analysis ; Female ; Humans ; Immunohistochemistry ; Lung ; pathology ; Male ; Middle Aged ; Nitric Oxide ; analysis ; Nitric Oxide Synthase Type II ; analysis ; Pneumonia ; etiology ; pathology ; Pulmonary Emphysema ; pathology ; Pulmonary Fibrosis ; pathology ; Sputum ; cytology