Occupational disease hazards in plywood manufacturing mainly include wood dust, formaldehyde, phenol, ammonia, noise, terpene, microorganisms, etc. The exposure is complex with multiple factors accompanied or coexisted. In the production process, these factors are exceeded, and mass occupational disease hazard events occurred among workers. Exposure to wood dust, formaldehyde, terpene, etc., put workers at increased risk of cancer. This article provides a review of this issue in order to provide a scientific basis for the prevention and control of occupational disease hazards in plywood manufacturing.
Humans ; Wood/chemistry* ; Occupational Diseases/chemically induced* ; Formaldehyde/adverse effects* ; Terpenes ; Dust ; Occupational Exposure/adverse effects*

Formaldehyde is a low molecular weight chemical and can elicit acute and chronic health related problems. Most of the inhaled formaldehyde is retained in the upper respiratory tract due to its extraordinary solubility. Therefore, cases of formaldehyde-induced occupational asthma are sporadic despite its widespread use in industrial processes. We herein report upon a case of occupational asthma due to formaldehyde, which was confirmed by workplace challenge including working environmental assessments, and by formaldehyde inhalation challenge using a specially designed closed-circuit apparatus. To investigate the possible involvement of an IgE-mediated mechanism, both in vitro and in vivo tests were done. IgE antibody specific for formaldehyde-human serum albumin conjugate (F-HSA) was not detected by ELISA, and no specific cutaneous reactivity to F-HSA was noted by either skin prick or intradermal test. The patient was diagnosed with formaldehyde-induced occupational asthma not associated with an IgE mediated mechanism.
Adult ; Antibodies/blood ; Asthma/*chemically induced ; Case Report ; Formaldehyde/*adverse effects/immunology ; Human ; Male ; Occupational Diseases/*chemically induced

The aim of this study was to determine whether formalin reliably provokes a paw edema and pain behavior. The paw of male Sprague-Dawley rats were injected with 100 microliter of formalin with 2.5% (F2.5), 5% (F5), and 10% (F10) concentrations. Following the formalin (n=8) or saline (control, n=6) injection, the flinching or licking of the paw was recorded for the phase 1 response (0-5 min after injection) and phase 2 response (20-60 min). The formalin-induced paw edema was assessed by measuring the diameters of the injected paws at 4 hr after injection. As for flinching, phase 1 and 2 of all three groups showed higher frequency than those of the control group (p<0.05). As for licking, phase 1 cumulative time of the F2.5 and F10 groups, and phase 2 cumulative time of the F2.5 and F5 groups showed a longer duration than those in the control group (p<0.05). The diameters of the paw in the F10 group were significantly larger than those in the control group (p<0.05). Flinching behavior was more reliably expressed the biphasic response than licking response at all formalin concentrations. Peak of the licking was reached at 2.5% and that of flinching was reached at 5%, whereas the paw edema peaked at 10% concentration. This suggests that there may be some dissociation of nociception from the edema formation.
Animals ; *Behavior, Animal ; Edema/*chemically induced ; Extremities ; Formaldehyde/*adverse effects ; Male ; Pain/*chemically induced ; Rats ; Rats, Sprague-Dawley

OBJECTIVETo investigate whether formalin inflammatory pain can induce the change in heme oxygenase-1 (HO-1) expression in the spinal cord of rats or not and the time course character.

METHODS42 SD rats were divided into 7 groups (n = 6): control formalin 6 h, formalin 12 h, formalin 1 d, formalin 2 d, formalin 3 d and formalin 7 d groups. Rats were subcutaneously injected with 0.2 ml 0.5% formalin into the ventral surface of right hind paw to induce periphery inflammatory pain. The immunohistochemistry was used to observe the expression of HO-1 protein in laminae I - II of the spinal cord dorsal horn and the area around canalis centralis of the I5 spinal segment of rats.

RESULTSThere are rare HO-1 immunoreactive cells in the laminae I - II of the dorsal horn and the area around canalis centralis of the I5 spinal segment of rats of control group and HO-1 immunoreactive cells were light in staining degree. Comparing with control group, the numbers of HO-1 immunoreactive cells in the I - II laminae of dorsal horn and area around canalis centralis were increased in the rats at 6 h after formalin injection. The number and staining degree of HO-1 immunoreactive cells were further increased at 12 h and peaked at 1 d after formalin injection. They didn't return to normal level at the 7th day. There were no difference in right and left dorsal horn in the number and staining degree of HO-1 immunoreactive cells at the same time after formalin injection.

CONCLUSIONFormalin inflammatory pain induced increased expression of HO-1 in the spinal cord dorsal horn and the area around canalis centralis of rats. At 1 d after injection of formalin, the increased expression of HO-1 was the most obviously.

Animals ; Formaldehyde ; adverse effects ; Heme Oxygenase (Decyclizing) ; metabolism ; Male ; Pain ; metabolism ; Pain Measurement ; Rats ; Rats, Sprague-Dawley ; Spinal Cord ; metabolism

OBJECTIVETo investigate the effects of occupational exposure to formaldehyde on the micronuclei frequencies in peripheral blood lymphocytes of workers.

METHODSTwo hundred thirty six plywood workers were divided into 3 exposure groups (low, middle and high) according to internal exposure biomarker (formaldehyde human serum albumin conjugate, FA-HSA), which was detected by ELISA. The concentrations of formaldehyde (FA) in air of two workshops were measure using the high performance liquid chromatography. Cytokinesis-block micronucleus (CBMN) test was used to detect the micronuclei frequencies of peripheral blood lymphocyte in 236 workers.

RESULTSThe average concentrations of FA in the low and high exposure workshops were 0.58 +/- 0.20 and 1.48 +/- 0.61 mg/m3, respectively, there was significant difference (P < 0.01). The average concentrations of serum FA-HAS of workers in two workshops were 69.22 +/- 15.37 and 136.29 +/- 89.49 pg/ml, respectively, there was significant difference (P < 0.01). The results of CBMN test showed that the micronucleus frequencies in low, middle and high exposure groups were 1.94 +/- 1.72, 2.10 +/- 1.92 and 2.10 +/- 1.70 per thousand, respectively, there were no significant differences between groups. However, the micronucleus frequencies in accumulative low, middle and high exposure groups were 1.36 +/- 1.36, 2.31 +/- 1.81 and 2.49 +/- 1.92 per thousand, respectively, there were significant differences between different accumulative exposure groups (P < 0.01). The results of correlation analysis indicated that there was a positive correlation between accumulative exposure levels and micronucleus frequencies (r(s) = 0.321, P < 0.01). The accumulative exposure doses may be a risk factor for high micronucleus frequencies in workers exposed to FA (P(trend) = 0.002).

CONCLUSIONFA-HSA levels can serve as an internal exposure biomarker for assessing the exposure level of workers exposed to FA. Accumulative formaldehyde exposure resulted in an increase of micronuclei frequencies of peripheral blood lymphocyte in plywood workers.

Adult ; Asian Continental Ancestry Group ; Biomarkers ; blood ; Formaldehyde ; adverse effects ; blood ; Humans ; Lymphocytes ; cytology ; drug effects ; Micronucleus Tests ; Occupational Exposure ; analysis ; Respiratory Hypersensitivity ; blood

OBJECTIVETo investigate the effect of formaldehyde exposure on the expression of inflammatory cytokines in human bronchial epithelial cells (16HBE cells).

METHODS16HBE cells were treated with formaldehyde with a concentration of 0, 0.04, 0.08, 0.16, 0.32, or 0.64 mmol/L for 24 hours, and MTT assay was applied to measure proliferative activity and calculate median lethal dose; 16HBE cells were exposed to formaldehyde with a concentration of 0, 0.04, 0.16, 0.64, or 1.20 mmol/L for 4 hours, MTT assay was applied to measure proliferative activity, and enzyme-linked immunosorbent assay was applied to measure the levels of Th1, Th2, and Th17 cytokines and tumor necrosis factor α(TNF-α) in cell supernatant.

RESULTSCompared with the control group, the 0.32-and 0.64-mmol/L exposure groups had significant decreases in cell viability (P<0.05); all exposure groups had reductions in interleukin(IL)-2 and IL-12, but no significant changes in interferon-γ and IL-10. In the 1.20-mmol/L exposure group, there was an increase in IL-4, with the increasing exposure dose, IL-5 and IL-6 tended to increase first and then decrease, and there was no significant change in IL-13; with the increasing exposure dose, IL-8 tended to increase first and then decrease, and there was no significant change in IL-17. In all the exposure groups, TNF-α increased and tended to increase significantly with the increasing exposure dose(P<0.05).

CONCLUSIONFormaldehyde exposure can cause imbalance between Th1 and Th2 cytokines secreted by 16HBE cells, as well as increased expression of IL-8 and TNF-α.

Cells, Cultured ; Cytokines ; metabolism ; Epithelial Cells ; drug effects ; metabolism ; Formaldehyde ; adverse effects ; Humans ; Interferon-gamma ; metabolism ; Interleukins ; metabolism ; Tumor Necrosis Factor-alpha ; metabolism

AIMTo observe the changes of nitric oxide synthase (NOS) activity and nitric oxide (NO) content of hippocampus including their time course and region distribution character in rat during the process of formalin-induced inflammatory pain as well as the pain behavior of rat.

METHODSThe pain threshold (PT) was determined by radiant heat-induced tail flick test. NOS expression in the hippocampus was determined by using NADPH-d histochemical staining. NO production in hippocampus was determined by assaying NO3- and NO2-.

RESULTSSubcutaneous injection of formalin elicited nociceptive behavioural response and led to decrease in PT of rat. The number and staining degree of NADPH-d positive neurons began to increase at 6 h after the formalin injection in CA1, CA2 - 3 and DG of hippocampus as well as NO content, which increased most obviously at 12 h and returned to control level at 48 h.

CONCLUSIONFormalin-induced inflammatory pain could induce the elevation of NOS activity in CA1, CA2 - 3 and DG of hippocampus with a certain time course, which further led to a increase of NO production in hippocampus.

Animals ; Formaldehyde ; adverse effects ; Hippocampus ; metabolism ; Inflammation ; chemically induced ; metabolism ; Male ; Nitric Oxide ; biosynthesis ; Nitric Oxide Synthase ; metabolism ; Pain ; chemically induced ; metabolism ; Pain Threshold ; Rats ; Rats, Sprague-Dawley

AIMTo observe the changes of cyclooxygenase-2 (COX-2) expression and especially the time course of the changes in dorsal horn of the spinal cord during formalin-induced inflammatory pain and hyperalgesia in rats.

METHODSCOX-2 immunohistochemistry staining was used in rat formalin pain model.

RESULTSCompared with control group the number and immunostaining density of COX-2 immunoreactive cells in the laminae I-VI of the dorsal horn of the spinal cord increased significantly 4 h, 1 d and 3 d after formalin injection (P < 0.05). The most obvious increase was observed 1 d after the injection.

CONCLUSIONCOX-2 in the dorsal horn of the spinal cord is involved in the formalin-induced inflammatory pain and hyperalgesia.

Animals ; Cyclooxygenase 2 ; metabolism ; Formaldehyde ; adverse effects ; Pain ; chemically induced ; metabolism ; Posterior Horn Cells ; metabolism ; Rats ; Rats, Sprague-Dawley ; Spinal Cord ; metabolism

Although formaldehyde is well known to cause type 4 hypersensitivity, immunoglobulin E (IgE)-mediated hypersensitivity to formaldehyde is rare. Here, we report a case of recurrent generalized urticaria after endodontic treatment using a para-formaldehyde (PFA)-containing root canal sealant and present a review of previous studies describing cases of immediate hypersensitivity reactions to formaldehyde. A 50-year-old man visited our allergy clinic for recurrent generalized urticaria several hours after endodontic treatment. Prick tests to latex, lidocaine, and formaldehyde showed negative reactions. However, swelling and redness at the prick site continued for several days. The level of formaldehyde-specific IgE was high (class 4). Thus, the patient was deemed to have experienced an IgE-mediated hypersensitivity reaction caused by the PFA used in the root canal disinfectant. Accordingly, we suggest that physicians should pay attention to type I hypersensitivity reactions to root canal disinfectants, even if the symptoms occur several hours after exposure.
Disinfectants/*adverse effects ; Formaldehyde/*adverse effects ; Humans ; Hypersensitivity, Immediate/*chemically induced ; Immunoglobulin E/*immunology ; Male ; Middle Aged ; Recurrence ; Skin Tests ; Time Factors ; Urticaria/*chemically induced/diagnosis ; Zinc Oxide-Eugenol Cement/*chemistry

OBJECTIVETo investigate the role of heme oxygenase and carbon monoxide (HO/CO) in the development of spontaneous pain and hyperalgesia of rats induced by formalin injection.

METHODSZinc protoporphyrin Znpp (the inhibitor of HO) was intrathecally injected to the rats with formalin inflammatory pain. Hemin (the agonist of HO) was intrathecally injected to the normal rats. The weighted pain scores were used to evaluate the degree of pain response. Thermal withdrawal latency and mechanical withdrawal threshold were observed to assess the degree of thermal hyperalgesia and mechanical allodynia.

RESULTSAfter the intrathecal injection of Znpp, the weighted pain score obviously reduced in a dose-dependent manner compared with the rats with formalin inflammatory pain. Intrathecal injection of Znpp had no obvious effect on thermal withdrawal latency and mechanical withdrawal threshold in injected feet compared with formalin group. But there was a prolongation in a dose-dependent manner in non injected feet. Intrathecal injection of Hemin to normal rats could shorten the thermal withdrawal latency and reduce the mechanical withdrawal threshold on both sides of hindpaws.

CONCLUSIONIntrathecal injection of the HO inhibitor produced prominent inhibition to pain related behavior and thermal and mechanical hyperalgesia induced by formalin injection. Intrathecal injection of HO inductor could induce thermal and mechanical hyperalgesia in normal rats. The results indicated that HO/CO took part in the processes of spinal cord nociceptive information transmission and the development of thermal and mechanical hyperalgesia.

Animals ; Carbon Monoxide ; Formaldehyde ; adverse effects ; Heme Oxygenase (Decyclizing) ; antagonists & inhibitors ; Hemin ; Hyperalgesia ; chemically induced ; Male ; Nociception ; Nociceptors ; drug effects ; physiology ; Pain ; chemically induced ; Protoporphyrins ; Rats ; Rats, Sprague-Dawley