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Metal working fluids: sub-chronic effects on pulmonary functions in B6C3F1 mice given vitamin E deficient and
Anna A Shvedova1, Elena Kisin, Ashley Murray
1Pathology and Physiology Research Branch, Engineering Control and Technology Branch, National Institute for Occupational Safety and Health, Centers for Disease Control and Prevention, Morgantown, WV 26505, USA. ats1@cdc.gov
Abstract:
Metal working fluids (MWFs) have been widely known to cause asthma and neoplasia of the larynx, pancreas, rectum, skin and urinary bladder (Textbook of Clinical Occupational and Environmental Medicine (1994) 814; Am. J. Ind. Med. 32 (1997) 240; Am. J. Ind. Med. 33 (1997) 282; Am. J. Ind. Med. 22 (1994) 185). Other non-neoplastic respiratory effects in industrial workers attributed to MWFs include increased rates of cough, phlegm production, wheeze, chronic bronchitis and chest tightness (Eur. J. Resir. Dis. 63(118) (1982), 79; J. Occup. Med. 24 (1982) 473; Am. J. Ind. Med. 32 (1997) 450). The epidemic and endemic nature of immune mediated lung morbidity commonly known as hypersensitivity pneumonitis in workers from several different industries using MWFs has been well documented (J. Allergy clin. Immunol. 91 (1993) 311; Chest 108 (1995) 636; MMWR45 (1996) 606; Am. J. Ind. Med. 32 (1997) 423). We studied morphological/functional and antioxidant outcomes in lungs after inhalation exposure of vitamin E deficient mice to MWF (27 mg m(-3) 17 weeks, 5 days a week, 6 h a day). Mice were given vitamin E deficient (<10 IU kg(-1) vitamin E) or basal diets (50 IU kg(-1) vitamin E) for 35 weeks. Inhalation exposure to MWF started after 18 weeks on diet. Microscopic observation of lungs from mice given vitamin E deficient or sufficient diets revealed no inflammation or morphological alteration after exposure to MWF. Mice given vitamin E deficient diet exhibited a significant decrease (P<0.05) in breathing rate, peak inspiratory/expiratory flow, minute ventilation, and tidal volume compared with sufficient controls. However, no differences were found after exposure to MWF in pulmonary function, with the exception of tidal volume which also significantly decreased (P<0.05). Exposure to MWF reduced vitamin E, protein thiol and ascorbate level in lungs. Exposure to MWF in combination with a vitamin E deficient diet resulted in significantly enhanced accumulation of peroxidative products compared with vitamin E deficient controls. This is the first report that describes the increase of oxidative stress in the lungs after MWF exposure.
Insights
Metal working fluids (MWFs) can cause respiratory issues. Vitamin E deficiency combined with MWF inhalation significantly increases oxidative stress in mouse lungs, impacting lung function.
Area of Science:
- Occupational Health
- Toxicology
- Pulmonary Medicine
Background:
- Metal working fluids (MWFs) are linked to respiratory diseases like asthma and hypersensitivity pneumonitis.
- Previous studies indicate MWFs cause non-neoplastic respiratory effects and various cancers.
Purpose of the Study:
- To investigate the effects of MWF inhalation on lung morphology, function, and antioxidant status in vitamin E deficient mice.
- To determine if vitamin E deficiency exacerbates MWF-induced lung injury and oxidative stress.
Main Methods:
- Vitamin E deficient or sufficient mice were exposed to MWF via inhalation for 17 weeks.
- Pulmonary function tests, lung morphology, and antioxidant levels (vitamin E, thiol, ascorbate) were assessed.
- Peroxidative products were measured to evaluate oxidative stress.
Main Results:
- MWF inhalation did not cause inflammation or morphological changes in mouse lungs, regardless of diet.
- Vitamin E deficient mice showed decreased pulmonary function (breathing rate, flow, ventilation, tidal volume) even before MWF exposure.
- MWF exposure reduced lung vitamin E, thiol, and ascorbate levels.
- Combined MWF exposure and vitamin E deficiency significantly increased peroxidative products in the lungs, indicating enhanced oxidative stress.
Conclusions:
- MWF inhalation increases oxidative stress in the lungs.
- Vitamin E deficiency exacerbates MWF-induced oxidative stress and negatively impacts lung function.
- This study highlights the role of oxidative stress in MWF-related lung injury.
