ArticleInhalation toxicology2014
Neurotoxicity following acute inhalation of aerosols generated during resistance spot weld-bonding of carbon steel.
Article in Inhalation toxicology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 19 citations in OpenAlex.
- Molecular Mechanisms Underlying Neuroinflammation Elicited by Occupational Injuries and Toxicants.International journal of molecular sciences · 2023Review
- Manganese Pollution and Its Remediation: A Review of Biological Removal and Promising Combination Strategies.Microorganisms · 2022Review
- Biological effects of inhaled crude oil vapor V. Altered biogenic amine neurotransmitters and neural protein expression.Toxicology and applied pharmacology · 2022Article
- Effects of Simultaneous Exposure to Smoking and Welding Fume on Pulmonary Function Tests in Spot Welders.Tanaffos · 2021Article
- Biological effects of inhaled hydraulic fracturing sand dust VII. Neuroinflammation and altered synaptic protein expression.Toxicology and applied pharmacology · 2020Article
- Low-Cost, Distributed Environmental Monitors for Factory Worker Health.Sensors (Basel, Switzerland) · 2018Article
- Aerosol characterization and pulmonary responses in rats after short-term inhalation of fumes generated during resistance spot welding of galvanized steel.Toxicology reports · 2017Article
- Manganese Is Essential for Neuronal Health.Annual review of nutrition · 2015Review
- Effects of acute inhalation of aerosols generated during resistance spot welding with mild-steel on pulmonary, vascular and immune responses in rats.Inhalation toxicology · 2014Article
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Authors and funding
13 authors at 1 institution in 1 country.
Funding
Abstract
Welding generates complex metal aerosols, inhalation of which is linked to adverse health effects among welders. An important health concern of welding fume (WF) exposure is neurological dysfunction akin to Parkinson's disease (PD). Some applications in manufacturing industry employ a variant welding technology known as "weld-bonding" that utilizes resistance spot welding, in combination with adhesives, for metal-to-metal welding. The presence of adhesives raises additional concerns about worker exposure to potentially toxic components like Methyl Methacrylate, Bisphenol A and volatile organic compounds (VOCs). Here, we investigated the potential neurotoxicological effects of exposure to welding aerosols generated during weld-bonding. Male Sprague-Dawley rats were exposed (25 mg/m³ targeted concentration; 4 h/day × 13 days) by whole-body inhalation to filtered air or aerosols generated by either weld-bonding with sparking (high metal, low VOCs; HM) or without sparking (low metal; high VOCs; LM). Fumes generated under these conditions exhibited complex aerosols that contained both metal oxide particulates and VOCs. LM aerosols contained a greater fraction of VOCs than HM, which comprised largely metal particulates of ultrafine morphology. Short-term exposure to LM aerosols caused distinct changes in the levels of the neurotransmitters, dopamine (DA) and serotonin (5-HT), in various brain areas examined. LM aerosols also specifically decreased the mRNA expression of the olfactory marker protein (Omp) and tyrosine hydroxylase (Th) in the olfactory bulb. Consistent with the decrease in Th, LM also reduced the expression of dopamine transporter (Slc6a3; Dat), as well as, dopamine D2 receptor (Drd2) in the olfactory bulb. In contrast, HM aerosols induced the expression of Th and dopamine D5 receptor (Drd5) mRNAs, elicited neuroinflammation and blood-brain barrier-related changes in the olfactory bulb, but did not alter the expression of Omp. Our findings divulge the differential effects of LM and HM aerosols in the brain and suggest that exposure to weld-bonding aerosols can potentially elicit neurotoxicity following a short-term exposure. However, further investigations are warranted to determine if the aerosols generated by weld-bonding can contribute to persistent long-term neurological deficits and/or neurodegeneration.
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