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Biomonitoring Exposure Thiab Kev Ntsuam Xyuas Thaum Ntxov hauv Silicosis: Kev Tshawb Fawb Txog Cov Ntaub Ntawv Tam Sim No

Oct 23, 2023

Abstract: Silicosis yog ib hom mob ntsws fibrosis uas tshwm sim los ntawm kev ua haujlwm raug rau crystalline silica. Kev ua haujlwm raug rau crystalline silica kuj ua rau muaj kev pheej hmoo ntawm cov kab mob ntsws ntev (COPD), mob qog noj ntshav, thiab mob ntsws, tshwj xeeb tshaj yog mob ntsws ntsws. Silicosis tam sim no tau kuaj pom hauv cov neeg ua haujlwm yav dhau los los ntawm cov qauv hauv siab X-ray thaum pom qhov txhab thiab rov qab tsis tau. Yog li ntawd, nws yuav tsum tau nrhiav cov cim tshwj xeeb thiab tsis cuam tshuam uas tuaj yeem kuaj xyuas silicosis nyob rau theem ua ntej, ua ntej tshwm sim ntawm X-ray opacities. Hauv cov lus piav qhia no, peb nthuav qhia ntau yam kev kuaj mob, saib xyuas thiab kwv yees biomarkers nrog lub peev xwm loj hauv kev tswj hwm ntawm silicosis, xws li pro- thiab anti-inflammatory cytokines (TNF (Tumour necrosis factor-), IL-1} (Interleukin{ {7}}), IL-6, IL-10), CC16 (Clara cell 16, indirect marker of epithelial cell destruction), KL-6 (Krebs von den Lungen 6, an indirect marker ntawm alveolar epithelial puas), neopterin (qhov taw qhia ntawm cellular tiv thaiv kab mob) thiab MUC5B noob (Mucin 5B, gel-forming mucin hauv mucus). Cov kev tshawb fawb tau pom tias tag nrho cov cim tau hais tseg saum toj no muaj peev xwm ua tau zoo rau kev kuaj mob ntxov lossis kev ntsuam xyuas ntawm kev nce qib hauv silicosis thiab sawv cev rau kev cog lus rau lwm txoj hauv kev hluav taws xob. Peb txiav txim siab tias yuav tsum muaj kev tshawb fawb ntau qhov chaw los soj ntsuam cov biomarkers nyob rau hauv kev sib raug zoo nrog kev ua haujlwm keeb kwm, kev kuaj mob histopathological, cov cim qhia, thiab kev kuaj mob ntsws rau cov pab pawg loj ntawm cov ncauj lus kom zoo dua qhov tseeb ntawm cov khoom siv biomarkers.

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Ntsiab lus: silicosis; biomarkers; Kev kuaj mob ntxov; kev saib xyuas; keeb kwm ua haujlwm

1. Taw qhia

Silicosis is a collagenous pneumoconiosis caused by long-term exposure to crystalline silica-rich dust. More precisely, silicosis is a type of pulmonary fibrosis caused by inhaled silica particles [1]. For crystalline silica particles to be biologically active, they must be small enough ("respirable") to reach the distal airways and alveoli; [2] therefore, their diameter should be less than 5 µm [3]. In addition, the concentration of crystalline silica in inhaled particles must reach a certain threshold (usually >10%), thiab lub sij hawm raug yuav tsum yog tsawg kawg yog 5 xyoo [1]. Txoj kev loj hlob ntawm silicosis yog ib qho kev mob ntev thiab kev loj hlob; yog li ntawd, thaum nws tshwm sim, nws yog irreversible. Muaj ntau tus cwj pwm ntawm tus kheej thiab tus cwj pwm uas ua rau muaj kev pheej hmoo tshwm sim, xws li cov kab mob ua ntej ua ntej ntawm txoj kev ua pa (pulmonary tuberculosis, chronic rhinitis, bronchitis, thiab lwm yam), genetic polymorphisms, haus cawv, haus luam yeeb, thiab kev ua si lub cev [1 ,4] ib.

2. Ua haujlwm raug

Crystalline silica yog tus neeg sawv cev etiological koom nrog kev txhim kho ntawm silicosis. Nws yog ib qho ntxhia nyob hauv lub ntiaj teb pob zeb, [5] qhov twg nws tshwm sim hauv ob hom: crystalline (quartz) thiab amorphous (diatom) [1]. Ob qho tib si crystalline thiab amorphous cov ntaub ntawv hloov mus rau hauv tridymite ntawm qhov kub thiab txias (800-1000 ◦C), uas, nyob rau hauv lem, raug rau kub ntau dua (1100–1400 ◦C), transforms rau hauv cristobalite. . Cov peb daim ntawv no (quartz, tridymite, cristobalite) yog lub ntsiab aetiological cov neeg sawv cev ntawm silicosis, uas nws fibrogenic muaj peev xwm nce nyob rau hauv qhov kev txiav txim hais. Hauv Romania, qhov txwv qhov tseem ceeb ntawm qhov raug rau quartz yog 1 mg / m3, thaum rau tridymite thiab cristobalite, tus nqi yog 0.5 mg / m3 [1,2,4]. Lub koom haum National rau Kev Nyab Xeeb Kev Nyab Xeeb thiab Kev Noj Qab Haus Huv (NIOSH) pom zoo kom muaj kev txwv tsis pub tsawg dua 0.5 mg / m3 rau ib qho allomorphic duab [6]. Raws li Lub Tsev Haujlwm Saib Xyuas Kev Noj Qab Haus Huv Hauv Tebchaws, hauv Romania, silicosis tau sau npe txo qis ntawm cov neeg mob tshiab hauv 2019: 87 piv rau 149 xyoo 2018 thiab qeb thib ob hauv cov qauv kev mob hnyav. Tom qab ntawd, hauv 2021, qhov nce me ntsis ntawm tag nrho cov neeg mob tau pom: 55 piv rau 30 xyoo 2020. Nyob nruab nrab ntawm 1998 thiab 2021, tus nqi nruab nrab ntawm cov neeg mob silica tshiab yog 294.3 ib xyoos [7]. Cov kev tshawb fawb txog kab mob kis tau pom tias muaj crystalline silica raug cuam tshuam nrog kev tuag ntau ntxiv thiab cov kab mob morbidity [8] vim yog silicosis, kab mob ntsws ntev (COPD), thiab mob ntsws cancer [9]. Thoob plaws ntiaj teb, xyoo 2019, 655.7 txhiab xyoo kev xiam oob qhab-hloov lub neej tau raug ntaus nqi rau silicosis [10]. Hauv 2017, 23,695 tus neeg mob silicosis tau tshaj tawm thoob ntiaj teb. Nyob nruab nrab ntawm xyoo 1990 thiab 2017, qee thaj chaw hauv cheeb tsam tau tshaj tawm qhov txo qis ntawm cov neeg mob silicosis (feem ntau nyob hauv Europe), tab sis qee thaj chaw xws li North thiab South Africa, Tuam Tshoj, thiab sub-Saharan Africa tau tshaj tawm txog kev nce siab [11]. NIOSH txheeb xyuas cov haujlwm hauv qab no raws li cov haujlwm uas muaj kev pheej hmoo: (1) kev tsim cov iav, tais diav, ceramics, cib, pob zeb thiab pob zeb dag, (2) abrasive blasting, (3) kev tsim khoom, (4) hydraulic fracturing, (5) stonecutting. thiab pob zeb countertop, (6) pob zeb drilling, (7) chaw txua txiag zeb, (8) tunneling, (9) kev tsim kho, (10) mining, (11) roj thiab roj extraction thiab (12) kho hniav [6]. Muab cov kev hloov pauv ntawm tib neeg thiab cov txheej txheem thev naus laus zis, cov kws kho mob yuav tsum tau saib xyuas tshwj xeeb hauv kev kuaj mob silicosis ob qho tib si hauv cov kev lag luam yav dhau los, txawm tias qee qhov ntawm lawv tau ploj mus hauv qee lub tebchaws (xws li mining, foundries) thiab hauv cov uas tau muab tso rau hauv cov tshiab tshiab. cov hauj lwm uas tshwm sim (xws li, sandblasting ris tsho hauv qab, dag pob zeb benchtop) [9,12].

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3. Cov ntaub ntawv thiab cov txheej txheem

Kab lus no yog cov lus piav qhia tsim los ntsuas thiab nthuav qhia ntau yam kev kuaj mob, kev soj ntsuam, thiab kev kwv yees biomarkers siv rau cov neeg mob uas muaj kev ua haujlwm raug rau crystalline silica. Rau qhov kev tshuaj xyuas no, cov ntaub ntawv uas twb muaj lawm raug xaiv los ntawm ntau cov ntaub ntawv xws li Pubmed, Scopus, ScienceDirect, thiab Google Scholar. Tom qab kev tshuaj xyuas zoo raws li pom hauv daim duab 1 (n=138 274 cov ntawv), peb tau xaiv 33 cov kev tshawb fawb uas tau nthuav tawm hauv Table 1, tsom mus rau kev kawm cov cim los ntsuas kev kuaj mob ntxov thiab kev loj hlob ntawm silicosis. Cov cytokines (TNF- (tumor necrosis factor-), IL-1 (Interleukin-1), IL-10, IL-6), CC16 (Clara cell 16), KL -6 (Krebs von den Lungen 6), MUC5B (Mucin 5B) noob thiab neopterin raug xaiv los ua cov ntsiab lus txaus siab rau kev tshawb nrhiav ntxiv. Peb siv cov npe ntawm cov cim uas tau hais los saum no ua raws li cov lus "silicosis", "mob", "anti-inflammatory", "immune dysregulation", "physiopathology", "evolution", "thaum ntxov kuaj", "genetic polymorphisms", thiab. "kev kho mob" nyob rau hauv txawv permutations. Rau txhua yam khoom, peb tau sau tseg cov txheej txheem lom neeg siv cov tshuab tshawb fawb tau piav qhia saum toj no thiab cov ntaub ntawv hauv tebchaws. Tom qab ntawd peb tau nthuav tawm cov kev xaiv ntawm cov kev tshawb fawb soj ntsuam thiab kev sim uas tau soj ntsuam ntau lub biomarkers rau lawv cov txiaj ntsig zoo hauv kev kuaj mob ntxov thiab kev hloov pauv ntawm silicosis. Peb tsis txwv lub sijhawm, txawm hais tias kev tshawb fawb tsis ntev los no tau nyiam dua.

Figure 1. Flowchart of the literature search. Flowchart of the literature search.

Daim duab 1. Flowchart ntawm cov ntaub ntawv tshawb nrhiav. Flowchart ntawm kev tshawb nrhiav cov ntaub ntawv.

Table 1. Extraction table of the 33 articles include in the narrative review (TNF-Tumour necrosis factor, OR- Odds ratio, CI-Confidence interval, IL-Interleukin, CC16-Clara cell 16, BALF-Broncho-alveolar lavage fluid, FEV1 -Forced expiratory volume in 1 s, VC—Vital capacity, ELISA—Enzyme linked immunosorbent assay, KL-6—Krebs von den Lungen 6, SP-D—Serum surfactant protein D, MMP—Matrix metalloproteinase, MUC5B—Mucin 5B, CWP — Coal neeg ua haujlwm pneumoconiosis, NF-κB—Nuclear factor kappa B, iNOS—Inducible nitric oxide synthase, IHC—Immunohistochemistry, TEM—Kev xa hluav taws xob microscopy).

Table 1

Table 1. Cont.

Table 1. Cont.

Table 1. Cont.

Table 1. Cont.


4. Cov teebmeem kev noj qab haus huv

Silicosis yog tus kab mob pneumoconiosis ntau tshaj plaws thiab raug cais raws li kev tshawb pom hluav taws xob hauv ob pawg: yooj yim (<10 mm diameter opacities) and complicated (>10 mm diam opacities). Lub pathogenesis ntawm silicosis yog raws li peb txoj kev xav: kev puas tsuaj macrophage, o ua rau fibrosis, thiab kev tiv thaiv kab mob [4].

Kev puas tsuaj Macrophage muab lub hauv paus rau qhov pib ntawm o, fibrosis, thiab kev tiv thaiv kab mob. Crystalline silica hais yog phagocytosed los ntawm macrophages ua rau muaj ntau yam xwm txheej uas tam sim no, raws sijhawm raws li hauv qab no: (1) rupture ntawm phab ntsa phagosome nyob rau hauv qhov kev txiav txim ntawm lysosomes, (2) tso tawm cov ntsiab lus rau hauv macrophage cytoplasm, (3) ) disintegration ntawm cov macrophage, (4) tso tawm ntawm hais thiab enzymes mus rau hauv lub extracellular kua, (5) resumption ntawm cov txheej txheem. Thaum qhib los ntawm respirable-loj silica, cov macrophages yuav pib cov txheej txheem inflammatory, collagen hypersynthesis, thiab immunological txheej txheem (Daim duab 2) [1,4].


Figure 2. The role of presented biomarkers in silicosis pathogenesis


Daim duab 2. Lub luag haujlwm ntawm kev nthuav qhia biomarkers hauv silicosis pathogenesis

Muab hais tias qhov pib ntawm tus kab mob histopathological tsis muaj cov cim qhia hluav taws xob (yuav muaj qhov ncua sij hawm ntawm qhov pib histopathological thiab pom cov kab mob radiologically pom) [1,3], muaj peev xwm biomarkers pab tau rau kev kuaj mob ntxov. Peb tau sau cov ntsiab lus tseem ceeb tshaj plaws uas tau hais los saum no biomarkers, raws li tau hais los ntawm cov ntaub ntawv tshwj xeeb tam sim no.

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5. Biomarkers

5.1. TNF

Alveolar macrophages, thawj kab tiv thaiv tawm tsam txawv teb chaws, ingest inhaled silica, ua rau cell tuag thiab extracellular silica tso. Tom qab ntawd cov silica raug ntes los ntawm lwm cov macrophages, ua rau lub voj voog rov ua dua uas tswj cov txheej txheem inflammatory. Macrophages tso tawm ntau tus neeg nruab nrab xws li cytotoxic oxidants, arachidonic acid metabolites, thiab inflammatory cytokines nrog rau TNF- , thiab IL-1. Cov neeg kho kom haum xeeb no pib nkag mus ntawm cov hlwb inflammatory thiab induce lawv infiltration mus rau hauv lub alveolar phab ntsa, tso proteolytic enzymes thiab toxic oxygen derivatives, ua rau cell puas thiab puas tsuaj ntawm extracellular matrix [45]. TNF yog ib qho glycoprotein uas tsim los ntawm cov macrophages, tab sis kuj los ntawm lwm cov hlwb: mast hlwb, lymphocytes, fibroblasts, granulocytes, thiab NK (natural killer) hlwb [46]. Cov teebmeem ntawm TNF suav nrog kev ua kom cov neutrophils, macrophages, B thiab T lymphocytes, thiab stimulation ntawm immunoglobulin synthesis. Nws kuj induces qog cell tuag los ntawm necrosis los yog apoptosis thiab txhawb cov synthesis ntawm lwm yam cytokines: IL-1, IL-6, thiab IFN (Interferon). TNF- stimulates lub synthesis thiab deposition ntawm extracellular matrix thiab collagen synthesis, li no txhawb txoj kev loj hlob ntawm fibrosis [13]. Yog li, TNF- ua lub luag haujlwm tseem ceeb hauv kev tswj cov txheej txheem inflammatory los ntawm activating macrophages, stimulating zus tau tej cov inflammatory proteins (cytokines), thiab stimulating T lymphocytes [4]. TNF- tuav ob peb lub luag haujlwm tseem ceeb hauv silicosis, suav nrog ua rau muaj kev cuam tshuam ntawm cov hlwb inflammatory thiab tso tawm ntawm lwm cov cytokines [13]. Cov kev tshawb fawb pom tau tias TNF- qib tau nce siab ua ntej qhov pib ntawm cov tsos mob cuam tshuam nrog silicosis, ua rau TNF- qhov kev xaiv tseem ceeb rau kev kuaj mob ntxov [14,47]. Cov ntaub ntawv muab los ntawm ib txoj kev tshawb fawb uas suav nrog 30 kev tswj hwm (cov tib neeg noj qab haus huv), 28 tus neeg raug silica (tsis muaj kab mob), thiab 30 silica cov ntsiab lus tau qhia tias TNF- plasma qib tau nce siab hauv cov neeg ua haujlwm raug mob. (p <0.05) thiab ntau dua hauv cov neeg mob silicosis ntau dua li ntawm pawg neeg noj qab haus huv (p <0.01), ua pov thawj tias TNF- yog ib qho kev pab cuam hauv cov kab mob ntawm silicosis [13]. Cov ntaub ntawv pov thawj los ntawm TNF-tsis muaj nas, uas tiv thaiv kev txhim kho ntawm silica-induced fibrosis, txhawb lub tswv yim tias TNF- ua lub luag haujlwm tseem ceeb hauv kev txhim kho pulmonary fibrosis [16]. Kev tso tawm hauv zos ntawm IL-1 thiab TNF- ntawm kab lis kev cai ntawm monocytes thiab macrophages hauv tib neeg tau pom tias ua raws li kab mob pathogenesis [39]. Siv cov tshuaj TNF tshwj xeeb uas hloov NF-collagen (non-fibrillar), F-collagen (fibrillar), thiab P4H (Prolyl 4-}hydroxylase) gene teb (fibrogenic gene qhia theem), nws tau pom tias hauv quartz- kho cov kab lis kev cai cog qoob loo, piv rau kev tswj hwm, muaj kev tshaj tawm ntawm TNF thiab silica-induced sponge collagen ntau lawm [36]. Anti-TNF tuaj yeem txo silica-induced pulmonary o los ntawm kev txo qis NF-κB (nuclear factor kappa B), signaling, oxidative stress, thiab TNF-, qhia tias anti-TNF yuav siv los kho silica-induced ntsws raug mob [37]. Cov kev tshawb fawb yav dhau los tso qhov kev txhawb nqa polymorphisms ntawm TNF- hauv cov kab mob inflammatory thiab kis kab mob [4]. Tam sim no, tsis muaj ntaub ntawv sib txuas ntawm TNF polymorphism-txog qhov cuam tshuam rau kev kis kab mob thiab silicosis, [23,48] tab sis nws tseem qhib seb puas muaj kev koom tes ncaj qha, muab qhov cuam tshuam ntawm cov neeg mob silicosis rau pulmonary tuberculosis [4]. Ib qho kev tshuaj ntsuam meta-tshaj qhia tias TNF -308 (11 kev tshawb fawb) thiab -238 (8 kev tshawb fawb) polymorphisms cuam tshuam nrog kev cuam tshuam rau silicosis [17]. Peb qhov kev tshawb pom pom tias kuj muaj lwm yam TNF polymorphisms txuas rau silicosis. Corbett et al. tau txheeb xyuas qhov sib txuas ntawm TNF- polymorphisms -238 thiab -376 thiab mob hnyav silicosis [18]. Ib txoj kev tshawb fawb los ntawm cov neeg ua haujlwm hauv lub tuam txhab cement tau pom tias cov tib neeg uas muaj kev hloov pauv caj ces ntawm TNF -308 gene loci tau raug tsim los ua silicosis. Cov kev tshawb pom no tau txhawb nqa los ntawm ntau dua ntawm TNF- tsim los ntawm TNF -308 gene variation subjects (p=0.004) [19]. Zuag qhia tag nrho, cov kev tshawb fawb tau pom tias nce TNF- qib hauv cov neeg ua haujlwm silica-tawm yam tsis muaj cov tsos mob ntawm tus kab mob tuaj yeem yog qhov muaj peev xwm biomarker rau kev kuaj mob silicosis ntxov. Tseem muaj ob qhov teeb meem uas xav tau kev ntsuas ntxiv hauv kev txhais cov txiaj ntsig no. Ua ntej, genotyping ntawm TNF polymorphisms yuav tsum raug coj mus rau hauv tus account nyob rau hauv tag nrho cov kev tshawb fawb hais txog TNF raws li biomarker rau silicosis, raws li TNF tau pom los txiav txim siab rau cov kab mob silicosis, thiab tsim ib daim ntawv nyuaj (progressive loj fibrosis). Qhov thib ob, kev hloov kho tshiab ntawm TNF / TNF- yuav tsum tau siv. TNF yog thawj zaug ntaus nqi rau ob lub molecules, TNF-, ib qho monocyte-derived qog necrosis factor, thiab TNF--, lymphocyte-derived qog necrosis factor [46]. Tom qab ntawd, nyob rau ntawm Lub Xya Hli 17th International TNF Congress (17-21 Tsib Hlis 1998; Hyannis, Massachusetts), lub npe "TNF-" raug hloov mus rau "lymphotoxin-". Concomitantly, "TNF-" los ua ib lo lus tsis tsim nyog, nrog tib lub ntsiab lus raws li lub ntsiab lus qub, "TNF", uas tau rov tsim los ua lub npe cytokine [49]. Txawm hais tias nws tau hloov npe ntau dua 20 xyoo dhau los, TNF tseem siv los ua TNF- hauv ntau qhov kev tshawb fawb tam sim no, ua rau qee qhov kev nkag siab tsis zoo ntawm cov kws sau ntawv molecule xa mus. Hauv ib txoj kev tshawb fawb, kev kho TNF tau pom tias muaj peev xwm txo tau cov kab mob silica. Txawm li cas los xij, kev tshawb fawb soj ntsuam tau ploj lawm, thiab lub sijhawm no, peb tsis tuaj yeem xaus rau qhov ua tau zoo ntawm silicosis.

5.2. IB -1

Macrophages qhib los ntawm respirable-loj crystalline silica tsim cov neeg nruab nrab thiab pib cov txheej txheem inflammatory. IL-1 ua rau muaj kev sib koom ua ke nrog rau lwm cov cytokines pro-inflammatory, xws li TNF- thiab IL-6. Cytokines secreted los ntawm activated macrophages (IL-1, IL-6, IL-12, IL-18) ​​yuav tig nyiam thiab qhib T lymphocytes, ua rau stimulation ntawm B lymphocytes los ntawm tom kawg (ntawm IL-11 thiab IL{{10}}) thiab pib ntawm cov tshuaj tiv thaiv kab mob. Qhov kev pheej hmoo ntawm silica hais nyob rau hauv lub ntsws cov ntaub so ntswg induces ib tug mob ua rau tag nrho cov hlwb, kom muaj ib tug tsis tu ncua inflammatory txheej txheem [4]. Cov kev tshawb fawb tsiaj thiab kev sim tshuaj ntsuam xyuas pom tau tias TNF- thiab IL-1 yog ib qho tseem ceeb hauv kev tswj hwm ntawm fibrotic mediators hauv silicosis. Kev sib txawv ntawm tus kheej hauv IL-1 thiab TNF- ntau lawm txhawb nqa lub tswv yim tias silicosis thiab kev loj hlob mus rau nws daim ntawv nyuaj yog txuas nrog tus tswv tsev cov caj ces predisposition los tsim cov proteins, txij li hauv cov kab mob inflammatory, qee qhov sib txawv ntawm allelic tau pom. yuav overexpressed. Piv txwv li, IL-1 gene polymorphism (IL-1RA +2018) muaj kev ywj pheej thiab muaj feem cuam tshuam nrog kev cuam tshuam thiab qhov hnyav ntawm silicosis hauv cov neeg raug, yog li qhov tshwm sim ntawm silicosis tsis tsuas yog nyob ntawm qhov kev siv, ntev, thiab lub sij hawm ntawm raug tab sis kuj nyob rau ntawm cytokine polymorphism [24,39]. Cov txiaj ntsig no yog ua raws li qhov kev tshawb pom ntawm Yucesoy B li al., qhov twg IL -1RA +2018 tau nce ntau hauv cov neeg mob uas muaj mob hnyav thiab mob silicosis, qhia tias qhov sib txawv no feem ntau cuam tshuam rau cov kab mob susceptibility [39] . Ib txoj kev tshawb fawb tau ua los ntawm ib pawg ntawm 99 cov kev kawm uas raug rau crystalline silica nyob rau hauv ib tug Turkish ceramic cog pom tau nce qib ntawm kev kawm interleukins hauv cov ntshav, suav nrog IL-1, piv rau pawg tswj hwm ntawm 81 cov kev kawm. Ntxiv mus, cov neeg laus muaj cov ntshav siab ntau dua IL-1 qhov tseem ceeb piv rau cov menyuam yaus [20]. Kev tshawb fawb soj ntsuam kev sib raug zoo ntawm IL-1 qib hauv cov ntshav thiab raug rau crystalline silica pom muaj kev cuam tshuam tseem ceeb ntawm kev sib txuam ntawm cov silica pawg piv rau cov kev noj qab haus huv (p <0.05) [21,38]. Txawm hais tias homology ntawm IL-1 thiab IL-1 yog 27%, [50] lawv khi rau tib receptor, IL-1R1 (IL-1 hom 1 receptor), thiab induce tib lub cev muaj zog [50,51]. Li no, hauv silicosis, IL-1 koom nrog hauv collagen deposition thiab modulation ntawm PDGF (platelet-derived growth factor) kev ua [40]. Tsis tas li ntawd, txoj kev tshawb fawb tau ua los ntawm cov kab lis kev cai ntawm cov hlwb coj los ntawm cov nas lub ntsws cov ntaub so ntswg pom tau tias tom qab raug cov crystalline silica, IL-1 tau tso tawm sai sai los ntawm alveolar macrophages, txhawb kev tsim cov IL-1, yog li txhawb lub ntsws o. [41]. Ib sab ntawm TNF, cov txiaj ntsig tau pom tias IL-1 polymorphisms genotyping, tshwj xeeb tshaj yog IL-1RA +2018, tuaj yeem cuam tshuam txog qhov cuam tshuam thiab qhov hnyav ntawm silicosis. Kev sib raug zoo ntawm qib IL-1 thiab qhov ceev ntawm cov hluav taws xob opacities hauv cov neeg mob silica tau tshaj tawm hauv ib qho kev tshawb fawb thiab yuav tsum tau lees paub hauv lwm pawg. Yog li ntawd, kev tshawb fawb ntxiv rau cov pab pawg loj ntawm cov kev kawm yog xav tau txhawm rau txhawm rau txhawm rau siv IL-1 hauv kev saib xyuas tus kab mob thiab IL-1 hauv cov txheej txheem tshuaj xyuas ntawm cov neeg raug thiab txiav txim siab txog IL-1 polymorphisms txuas rau kev tsim silicosis.

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cistanche tubulosa- txhim kho lub cev tiv thaiv kab mob

5.3. IB -10

Anti-inflammatory cytokines yog ib pab pawg ntawm immunoregulatory molecules kho cov pro-inflammatory cytokine teb. Txhawm rau tswj lub cev tiv thaiv kab mob, cytokines ua ke nrog qee yam cytokine inhibitors thiab soluble cytokine receptors. Ib qho tseem ceeb tshaj plaws los tiv thaiv cytokines yog IL-10. IL-10 yog tus tswj hwm tseem ceeb ntawm kev sib txawv thiab kev loj hlob ntawm ntau lub cev tiv thaiv kab mob thiab kev ua kom zoo thiab txawm tias tiv thaiv kev mob tshwm sim [52]. Hauv silicosis, IL-10 nce siab tab sis muaj ob qho txiaj ntsig: ntawm ib sab, IL-10 txwv qhov amplitude ntawm cov lus teb inflammatory los ntawm kev tawm tsam ntawm kev tsim tawm IL-1 , IL{{9} } }, thiab TNF- hauv monocytes thiab macrophages [53]. Ntawm qhov tod tes, los ntawm inducing cov txheej txheem fibrotic, IL-10 pab txhawb rau qhov txuas ntxiv ntawm cov kab mob pneumoconiosis. Kurniawidjaja LM pib los ntawm kev xav tias cov txheej txheem inflammatory txhawb kev tsim tawm ntawm IL-10, uas muaj lub luag haujlwm tiv thaiv. Qhov TNF- dhau IL{16}} piv tau raug soj ntsuam, thiab cov txiaj ntsig tau pom qhov piv txwv tsawg dua 1 tau muaj kev tiv thaiv los ntawm kev txhim kho silicosis. Qhov kev piav qhia feem ntau yog tias cov tshuaj tiv thaiv kab mob ntawm IL-10 ntau dua qhov kev mob tshwm sim ntawm TNF- . Yog tias TNF- / IL-10 piv yog supraunitary, IL-10 tsis tuaj yeem cuam tshuam cov nyhuv pro-inflammatory ntawm TNF-, qhia tias qhov kev pheej hmoo ntawm silicosis yuav tsum tau muab los ntawm qhov piv no thiab tsis yog los ntawm tus nqi ywj pheej ntawm TNF- thiab IL-10. Qhov sib txawv tseem ceeb ntawm TNF- / IL-10 piv qhov tseem ceeb yog ywj siab ntawm TNF- genetic variation [49].

5.4. IB -6

IL {{0}} yog ib qho cytokine ntau yam thiab ua lub luag haujlwm tseem ceeb hauv kev mob thiab tiv thaiv kab mob. Hauv cov kab mob pulmonary, nce qib ntawm IL-6 muaj nyob rau hauv cov kua dej bronchoalveolar lavage, lub ntsws cov ntaub so ntswg, thiab ntshav. IL-6 pab txhawb lub ntsws infiltration nrog inflammatory hlwb los ntawm inducing cell qhia ntawm adhesion molecules ntawm inflammatory cells thiab plays lub luag hauj lwm nyob rau hauv regulating fibrosis los ntawm modulating qhia ntawm Th2 cytokines [54]. IL-6 tswj kev tsim tawm ntawm IL-1 thiab TNF- thiab yog lub npe hu ua tus neeg nruab nrab ntawm cov lus teb rau theem mob hnyav thiab tseem muaj cov tshuaj tiv thaiv kab mob. Nyob rau hauv lub xub ntiag ntawm TGF- (transforming kev loj hlob factor-), IL-6 inhibits kev loj hlob ntawm kev tswj T hlwb thiab txhawb Th17 sib txawv, uas ua rau IL-17 [16]. Braz NFT et al. thiab Blanco-Pérez JJ et al. tshawb xyuas ntau yam cytokines; ib qho ntawm cov kev tshawb pom loj ntawm ob txoj kev tshawb fawb yog tias cov ntshav qab zib ntau dua ntawm IL -6 tau pom nyob rau hauv cov neeg mob silicosis thiab hauv cov neeg uas raug crystalline silica ntau dua li cov neeg tsis noj qab haus huv [15,16]. Hauv kev tshawb fawb soj ntsuam tsis ntev los no, ib pawg ntawm cov neeg mob silicosis tau muab faib ua ob pawg los ntsuas qhov kev kho mob rau silicosis (acetylcysteine ​​+ tetrandrine) thiab nws cov nyhuv ntawm cov ntshav IL-6 thiab TNF- theem. Tetrandrine ua ke nrog N-acetylcysteine ​​​​ntau zaus siv los kho cov neeg mob hauv pawg soj ntsuam, thaum pawg tswj hwm tau txais cov qauv, kev kho mob. Ua ntej kho, tsis pom qhov txawv ntawm cov ntshav ntawm IL-6 thiab TNF- (p > 0.05) ntawm ob pawg tau pom. Tom qab kev kho mob, cov qib ntawm cov cytokines tau hais los saum toj no tau txo qis hauv ob pawg, tab sis hauv pab pawg soj ntsuam, qhov txo qis qis dua (p <0.05). Tetrandrine ua ke nrog acetylcysteine ​​​​tuaj yeem pab txhawb kev sib koom ua ke los txhim kho cov kev kho mob hauv silicosis thiab txo qhov mob hnyav. Cov txiaj ntsig kho mob tau raug soj ntsuam los ntawm kev txiav txim siab FVC (yuav tsum muaj peev xwm tseem ceeb), FEV1 (yuav tsum ntim ntim hauv 1 s), thiab RR (tus nqi ua pa). FVC, FEV1, thiab RR pom tau tias muaj kev txhim kho tom qab kho, tab sis tsis muaj kev sib raug zoo nrog lub hauv siab X-ray lossis xam tomography. Raws li cov txiaj ntsig no, cov kws sau ntawv tau xaus lus tias cov ntshav peripheral IL-6 thiab TNF- qib tseem ceeb rau kev tswj silicosis, thiab lawv qhov kev kuaj pom tuaj yeem txo cov X-rays raws li cov txheej txheem ua raws [22]. Nrog rau TNF- thiab IL-1, IL-6 tau ntev tau suav tias yog ib qho pro-inflammatory cytokine uas tsim los ntawm lipopolysaccharide. IL-6 feem ntau yog siv los ua ib qho cim ntawm kev ua haujlwm ntawm cov kab mob proinflammatory cytokine. IL-6 muaj cov yam ntxwv tiv thaiv kab mob thiab tiv thaiv kab mob, zoo li ntau lwm yam cytokines, nrog rau theem mob protein teb raug cuam tshuam los ntawm IL-6. IL-6 muaj qhov txo qis ntawm kev tsim cov tshuaj tiv thaiv kab mob cytokines, xws li IL-10 thiab TGF- , thiab txo qhov tso tawm ntawm pro-inflammatory cytokines. Ntxiv rau kev txhim kho IL-1Ra (IL-1 receptor antagonist) ntau lawm thiab soluble TNF receptor tso tawm, IL-6 nce glucocorticoid synthesis. IL-6 kuj tseem tiv thaiv cov synthesis ntawm pro-inflammatory cytokines xws li GM-CSF (granulocyte-macrophage colony-stimulating factor), IFN- , thiab MIP-2 (macrophage inflammatory protein-2) [55]. IL-6 tau pom cov txiaj ntsig tau zoo hauv kev kuaj mob silicosis, suav nrog nws theem pib, thaum opacities tsis pom hluav taws xob pom. Txawm li cas los xij, IL-6 yog cytokine secreted raws li cov lus teb nyob rau hauv ntau lwm yam inflammatory kev tshwm sim (kab mob, raug rau lwm yam hais, thiab lwm yam), thiab cov xwm txheej no yuav tsum tau muab tshem tawm nyob rau hauv tus neeg txiav txim ntawm no biomarker tseem ceeb. Hauv cov neeg mob uas tau kuaj mob silicotic lawm, qhov kev hloov pauv ntawm IL-6 tuaj yeem txo cov xoo hluav taws xob hauv siab thiab tuaj yeem siv los saib xyuas kev tswj tus kab mob.

5.5. CC 16

Clara cell protein (CC16) yog cov protein zais cia los ntawm Clara hlwb, nws lub npe los ntawm nws qhov hnyav molecular ntawm 16 kD. Nws yog feem ntau pom nyob rau hauv lub distal ua pa ib ntsuj av, tshwj xeeb tshaj yog nyob rau hauv lub davhlau ya nyob twg bronchioles [25,42,56]. Cov protein no muaj cov tshuaj tiv thaiv kab mob, tshuaj tua kab mob, tiv thaiv fibrotic, thiab lub luag haujlwm tiv thaiv kab mob [25,57]. Cov kab mob hauv cov hlab ntsws tuaj yeem ua rau txo qis ntawm Clara hlwb, thiab qhov kev txo qis tuaj yeem cuam tshuam cov cell epithelial puas thaum lub sijhawm [58]. Ntau qhov kev tshawb fawb tau txawm hais tias CC16 yog ib qho khoom siv peripheral biomarker ntawm lub ntsws epithelial puas [25–28]. Ntau theem ntawm Clara cell puas tuaj yeem ua rau txo qis hauv kev ua haujlwm, tshwj xeeb tshaj yog nyob rau hauv lawv lub peev xwm los tiv thaiv kab mob. Ib qho laj thawj uas tuaj yeem yog silica hmoov av muaj peev xwm ua rau lub ntsws puas tsuaj; raws li qhov mob no maj mam nce nrog lub sijhawm ntev, nws ua rau txo qis ntawm Clara hlwb los ntawm kev puas tsuaj ntawm tes. Cov tshuaj lom uas tso tawm los ntawm activated phagocytes thiab dawb radicals kuj yuav ua rau qhov kev puas tsuaj no [26]. Ib txoj kev tshawb fawb pom tau tias qhov txo qis hauv CC16 qib hauv BALF (Broncho-alveolar lavage kua) hauv pawg silicosis nrog me me opacities (<10 mm) compared to the control group [3,26]. Moreover, the authors reported lower CC16 levels in patients with simple silicosis compared to the group with complicated silicosis (progressive massive fibrosis) (p < 0.05) [3,26]. This result was attributed by the authors to a possible self-repair process of epithelial cells [26] but, to the best of our knowledge, without experimental evidence, such as a lung biopsy, to support the assumption. Another study comparing three groups (silicosis, exposed, and control group) showed that the serum levels of CC16 were lower in the silicosis group, followed by the exposed group, and the highest levels were in the control group (p < 0.001) [25]. A 2020 study suggests that a CC16 serum value below 7.0 ng/mL in workers with an occupational history of crystalline silica exposure could represent a potential marker for the detection of silicosis in the early stage [27]. Sarkar K et al. investigated the CC16 in the serum of 117 silicosis subjects and 32 nonexposed individuals. The results of the study showed an inversely proportional relationship between the degree of lung damage on chest X-rays and CC16 serum values. The study also suggests that a cut-off value of 9 ng/mL can be correlated with early silicosis [28]. Although the cut-off values of the two studies differ, it is a promising start in recruiting peripheral biomarkers for the diagnosis of early-stage silicosis. Considering the limitations discussed, more studies are needed to accurately determine the cut-off value of CC16, preferably on larger groups of subjects with different radiological stages. A study conducted on 106 subjects (68 silica-exposed and 38 healthy individuals) measured serum CC16 levels by two methods: ELISA (enzyme-linked immunosorbent assay), the standard reference method, and semi-quantitative lateral flow assay (immunochromatography). By ELISA, all subjects radiologically confirmed with silicosis had CC16 levels below 9 ng/mL, while healthy subjects showed CC16 > 9 ng/mL. In the semi-quantitative lateral flow assay, CC16 values were represented by ranges (<6 ng/mL, 6.1–9 ng/mL, >9 ng / mL), thiab cov txiaj ntsig los ntawm txoj kev no tau pom qhov rhiab heev ntawm 100% thiab qhov tshwj xeeb ntawm 95%, piv rau ELISA cov txiaj ntsig [29]. Cov kev tshawb pom no qhia txog txoj hauv kev tshiab rau kev tshawb nrhiav CC16, yog ib txoj hauv kev pheej yig dua thiab rov tsim dua tshiab, uas tuaj yeem siv tau yooj yim raws li kev tshuaj xyuas hauv txhua qhov kev cuam tshuam txog kev ua haujlwm silica, txawm tias nyob hauv thaj chaw tsawg dua. Txhua qhov kev tshawb pom tau pom tias cov ntshav qab zib thiab BALF CC16 qib hauv cov neeg mob silica tau qis dua hauv cov pab pawg tsis raug. Ntxiv mus, cov qib CC16 tau tshaj tawm kom txo qis raws li qib silicosis thiab cuam tshuam rau FEV1 / VC piv. CC16 kev tshawb pom los ntawm ib nrab-quantitative lateral flow assay yuav tsum tau siv rau cov pab pawg loj ntawm cov ncauj lus kom zoo dua kev ntsuas qhov rhiab heev thiab tshwj xeeb piv rau ELISA hauv cov neeg uas muaj silica.

5.6. KL -6

KL-6, tseem hu ua MUC-1 (Mucin 1), yog ib qho mucin-zoo li glycoprotein nrog qhov hnyav molecular thiab pom tau hais tias tau hais tawm ntawm hom 2 pneumocytes (feem ntau hauv cytoplasm thiab daim nyias nyias) [59,60], Clara cells thiab bronchial glands [61]. Niaj hnub no, nws tau paub tias nce qib ntawm KL-6 hauv cov ntshav ua rau muaj kev cuam tshuam ntawm alveolar epithelial puas tsuaj [62]. KL-6 tuaj yeem txhawb kev tsiv teb tsaws thiab kev loj hlob ntawm fibroblasts thiab inhibit programmed cell tuag (apoptosis). Yog li, KL-6 tuaj yeem ua rau pulmonary fibrosis [63]. KL-6 tso tawm los ntawm kev loj hlob ntawm hom 2 pneumocytes hauv pulmonary fibrosis ntsig txog kev ua haujlwm raug rau plua plav lossis fibers, raws li pneumoconioses, ua rau muaj kev nce ntxiv hauv KL-6 ntshav ntshav. Yog li, nws tuaj yeem txhawb nqa cov txheej txheem fibrotic hauv cov neeg mob uas muaj kab mob ntsws interstitial thiab nce qhov muaj peev xwm xav tau kev kho mob anti-KL{17}} antibody [64]. Ib txoj kev tshawb fawb hauv nas tau pom tias tom qab 45 hnub ntawm crystalline silica raug, pulmonary fibrosis tau pom tau thiab qib ntawm KL -6 hauv cov ntshav tau zoo cuam tshuam nrog qhov mob hnyav ntawm fibrotic lesions [43]. Cov ntaub ntawv ntawm tib neeg cov ntsiab lus tau pom tias cov ntshav qab zib KL-6 ntau dua hauv pneumoconioses dua li kev tswj hwm kev noj qab haus huv lossis cov neeg raug mob [30]. Yog li, cov txiaj ntsig tshwj xeeb xa mus rau silica yog qhov tsawg. KL-6 yog lub peev xwm biomarker rau kev ua haujlwm-induced fibrosis thiab rau lub ntsws fibrosis, feem ntau. Lub luag haujlwm hauv kev kuaj mob silicosis tseem tsis tau txhais.

5.7. MUC5B noob

MUC5B noob encodes MUC5B protein, lub ntsiab gel-forming mucin nyob rau hauv tib neeg thiab nas mucus. Yog li, MUC5B pab txhawb rau lub lubrication thiab viscoelasticity ntawm lub ntsws, qaub ncaug, thiab ncauj tsev menyuam mucus [65]. Cov kev tshawb fawb pom tias MUC5B overexpression nyob rau hauv lub distal airways cuam tshuam qhov nyiaj tshuav uas yuav tsum tau los txhawb nqa mucociliary zoo, yog li cuam tshuam rau cov hnoos qeev. Qhov cuam tshuam ntawm MUC5B hauv kev txhim kho pulmonary fibrosis qhia ob qhov kev xav. Ua ntej, raug rau cov plua plav ua pa thiab microparticles, thiab tom qab ntawd lawv khaws cia hauv lub ntsws, tuaj yeem ua rau mucociliary ua haujlwm tsis zoo. Qhov thib ob, qhov mob tshwm sim los ntawm cov khoom khaws cia tuaj yeem sawv cev rau qhov pib ntawm collagen deposition los ntawm fibrotic microlesions. Lwm txoj kev xav rau qhov tshwm sim ntawm pulmonary fibrosis txuas rau MUC5B overexpression yog txhawb nqa los ntawm kev txo qis hauv lub ntsws tshem tawm thiab nce mucus viscosity [66]. Ib txoj kev tshawb fawb hauv nas tau pom tias cov khoom siv silica tuaj yeem ua tsis tau tsuas yog rau kev hloov pauv ntawm kev qhia ntawm MUC5B tab sis kuj ua rau cilia tsis ua haujlwm thiab ua rau hnoos qeev ntau dhau. Cov kev tshawb fawb ntxiv yog xav tau kom nkag siab zoo dua yog tias qhov kev tshawb pom no txuas ncaj qha rau silicosis thiab yuav tsum muaj cov ntaub ntawv hais txog MUC5B polymorphisms thiab lawv qhov cuam tshuam rau kev cuam tshuam ntawm silica-txog fibrosis [44]. Ib txoj kev tshawb fawb los ntawm cov neeg Suav pom tau hais tias MUC5B rs2672794 gene polymorphism yog nyob rau hauv kev sib raug zoo nrog cov miner pneumoconiosis, yog li MUC5B rs2672794 CC genotype tuaj yeem ua rau muaj kev pheej hmoo ntawm kev mob pneumoconiosis [31]. Raws li MUC5B yog cov noob caj noob ces feem ntau kawm rau nws lub luag haujlwm hauvmob ntsws fibrosis, nyob rau hauv kev tshawb fawb yav tom ntej, kev hloov pauv ntawm cov noob qhia hauv tib neeg los ntawm kev raug silica yuav tsum raug txiav txim siab.

5.8. Neopterin

Neopterin, ib tug pyrazinopyrimidine molecule uas belongs rau cov chav kawm pteridine, yog soluble nyob rau hauv plasma los yog serum thiab yog ib qho tseem ceeb thiab thaum ntxov qhia ntawm cellular tiv thaiv kab mob. Dendritic hlwb, macrophages, thiab monocytes uas tau raug txhawb los ntawm IFN- tsim neopterin. Neopterin yog ib qho tseem ceeb prognostic biomarker rau immunological stimulation, kab mob mus tas li, cell-mediated tiv thaiv, thiab oxidative kev nyuaj siab [67]. Lub neopterin secretion induced los ntawm IFN- yog txuas mus rau zus tau tej cov cytotoxic oxidants, ua neopterin ib tug neeg sib tw rau kev soj ntsuam oxidative kev nyuaj siab, tsis tsuas cellular tiv thaiv [32]. Cov qib neopterin hauv cov ntshav tuaj yeem siv los ua qhov taw qhia ntawm silica-kev cuam tshuam txog kev cuam tshuam thiab lwm yam kev ua haujlwm tsis zoo. Kev nce qib ntawm neopterin hauv cov ntshav ntawm cov neeg mob silicosis nce qhov ua tau ntawm nws qhov cuam tshuam hauv kev tiv thaiv kab mob ntawm tes thiab kev ua kom macrophage txuas ntxiv hauv cov kab mob pathogenesis [34]. Neopterin tuaj yeem suav tias yog lub peev xwm biomarker txhawm rau txheeb xyuas qhov teebmeem kev noj qab haus huv tshaj plaws ntawm crystalline silica [32]. Txawm li cas los xij, txhawm rau txhawm rau ua tiav hauv kev kho mob, kev tshawb fawb ntxiv yuav tsum tau tshawb xyuas oxidative kev ntxhov siab tsis zoo li neopterin [32]. Hauv kev tshawb fawb ntawm cov neeg ua haujlwm raug rau crystalline silica, qib siab dua tau pom nyob rau hauv cov ntaub ntawv raug piv rau cov tib neeg noj qab haus huv (p < 0.05). Cov txiaj ntsig tseem pom tau tias qhov nce neopterin qhov tseem ceeb hauv cov ntsiab lus raug cuam tshuam los ntawm kev muaj cov crystalline silica nyob rau hauv feem ua pa thiab tsis cuam tshuam los ntawm tus kheej yam ntxwv lossis lub sijhawm raug [35]. Txawm li cas los xij, txoj kev tshawb nrhiav kev tshawb fawb pib los ntawm cov lus piav qhia tsis tiav ntawm txoj kev, tsis suav nrog cov ntsiab lus 'qhov nruab nrab raug rau crystalline silica. Txoj kev tshawb no muab cov ntaub ntawv tsis tshua muaj tshwm sim, tshwj xeeb tshaj yog nyob rau lub sijhawm ntev. Cov ntaub ntawv tsuas yog tso siab rau ntawm qhov ua pa ntawm lub ntsws ntsuas ntawm lub sijhawm taw qhia, txawm hais tias cov ntsiab lus raug cuam tshuam rau qee kis tau dhau 20 xyoo. Lwm txoj kev tshawb fawb tau txais qhov sib txawv tseem ceeb hauv cov ntshav thiab cov zis neopterin theem ntawm cov neeg raug mob thiab cov neeg noj qab haus huv. Cov qib neopterin hauv cov zis thiab ntshav tau nce siab hauv cov neeg ua haujlwm silica. Kev nce qib neopterin hauv cov ntshav, zis, thiab lwm yam kua hauv lub cev tuaj yeem qhia txog qib ntawm kev tiv thaiv kab mob ntawm tes thiab kwv yees tus nqi ntawm oxidative stress [33]. Tag nrho cov kev tshawb fawb pom tau tias neopterin muaj peev xwm zoo li biomarker rau kev tshawb pom ntxov ntawm silicosis, tab sis, kom raug zoo dua, cov ntsuas oxidative kev ntxhov siab kuj yuav tsum tau ntsuas.

Desert ginseng—Improve immunity (2)

cistanche tubulosa- txhim kho lub cev tiv thaiv kab mob

6. Cov lus xaus

Silicosis tseem yog ib qho ntawm cov teeb meem kev noj qab haus huv tseem ceeb thoob plaws ntiaj teb. Muab cov ntsiab lus tam sim no uas qhov kev kuaj mob ntawm silicosis tsuas yog tsim los ntawm lub hauv paus ntawm kev hloov pauv hluav taws xob lig thiab hloov tsis tau, qhov tsis muaj cov biomarkers tshwj xeeb hauv kev soj ntsuam raws tu qauv ntawm cov neeg mob silica-exposed yuav tsim nyog.

Txhawm rau muab cov txiaj ntsig tau nthuav tawm rau hauv kev kho mob thiab cov txheej txheem kuaj mob rau cov neeg mob silicosis thaum ntxov, cov kev tshawb fawb ntxiv yuav tsum tau tshawb xyuas cov cytokine profile thiab kev ua haujlwm polymorphisms hauv cov neeg mob silicosis. Cov txiaj ntsig no yuav tsum muaj feem cuam tshuam nrog keeb kwm kev ua haujlwm (lub sijhawm raug mob, lub sijhawm khaws cia, sijhawm ntev, thiab qhov hnyav ntawm qhov tshwm sim), kev kuaj mob histopathological, kev kuaj pom, thiab cov txiaj ntsig ntawm kev ua haujlwm pulmonary. Ntxiv mus, cov txiaj ntsig no yuav tsum tau txhais hauv cov ntsiab lus kho mob thiab yuav tsum tsis suav nrog cov kab mob silica ntsig txog kev ua pa xws li kev mob ntsws ntsws thiab ua rau muaj mob hnyav. Txawm hais tias tag nrho cov kev tshawb pom pom muaj peev xwm loj heev rau kev kuaj mob ntxov ntawm silicosis, CC16 kev tshawb pom los ntawm immunochromatography zoo li qhov zoo tshaj plaws thiab yuav tsum tau siv rau cov pab pawg loj dua los ua kom pom qhov dav dav ntawm qhov kev nkag siab thiab tshwj xeeb ntawm txoj hauv kev rau yav tom ntej kev taw qhia rau kev kho mob. thiab soj ntsuam raws tu qauv.

Cov ntaub ntawv

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