The impact of wood dust on pulmonary function and blood immunoglobulin E, erythrocyte sedimentation rate, and C‐ reactive protein: A cross‐sectional study among sawmill workers in Tangail, Bangladesh

Abstract

Background and Aims: Occupational exposure to wood dust leads to lung function abnormalities that are prominent causes of morbidity and disability of sawmill workers. The adverse respiratory effects of wood dust in sawmills have not been studied thoroughly in Bangladesh. This study aimed to investigate the effect of wood dust on the respiratory health of sawmill workers compared to controls as well as to determine the association of wood dust-exposing effects with inflammatory blood biomarkers, such as immunoglobulin E (IgE), erythrocyte sedimentation rate (ESR), and C-reactive protein (CRP).Methods: This cross-sectional study included 100 sawmill workers from 25 distinct sawmills in various areas of Tangail, Bangladesh as well as 100 healthy volunteers who were adopted as a control group. Questionaries' survey and pulmonary function tests were performed face to face. Furthermore, after performing lung function tests, blood was drawn for further IgE, ESR, and CRP analyses.Results: Respiratory symptoms including breathlessness (32%), coughing (39%), sneezing (43%), chest tightness (30%), and itching (40%) were significantly higher in sawmill workers compared with control. Besides, sawmill workers' exposure to wood dust revealed a significantly lower level of spirometry parameters (forced vital capacity [FVC], FVC (%), forced expiratory volume in 1 s [FEV1], FEV1 (%), peak expiratory flow [PEF], PEF (%), FEV1/FVC (%), FEF25, FEF75, and FEF2575) compared with control and these spirometry parameters decreased with the increasing length of service. Moreover, a significantly higher level of IgE was observed in sawmill workers (290.90 ± 39.49) than in the control (120.95 ± 23.00).The high level of IgE suggests that the lower pulmonary function may be linked to allergic responses to wood dust among sawmill workers.

C-Reactive Protein: Pathophysiology, Diagnosis, False Test Results and a Novel Diagnostic Algorithm for Clinicians

“…such micro- or nanoparticles can be a constituent of environmental toxicity, which can also lead to low-grade inflammation, and except for smoking/passive smokers and smoke inhalation, which was previously discussed to increased CRP levels, air pollution has already been attributed to systemic inflammation and possibly increased CRP concentrations (i.e., exposed to PM2.5, fumes, home fireplaces/indoor pets/toxic metals, and other occupational-related exposures, such as wood dust, cotton, silica, asbestos, etc.) [ 1086 , 1087 , 1088 , 1089 , 1090 , 1091 , 1092 , 1093 , 1094 , 1095 , 1096 , 1097 , 1098 , 1099 , 1100 , 1101 , 1102 , 1103 , 1104 , 1105 ]. Finally, radiation from both the medical and the industrial field as well as through accidentally exposure can result into inflammation, and some data highlight an acute phase response caused by radiotherapy/radiochemotherapy, yet evidence toward CRP behavior in the extensive use of mobile phones, related devices, and other Wi-Fi wireless technologies seem sparse; nevertheless, some data on UV radiation indicate risks for possible systemic inflammation [ 1106 , 1107 , 1108 , 1109 , 1110 , 1111 , 1112 , 1113 , 1114 ].…”