Intense heat is produced during the welding process which can have a damaging effect on the welder’s health. These fumes cause a range of respiratory illnesses such as bronchitis or occupational asthma but they can affect other parts of the body as well.
One example is a condition called Manganese Poisoning and how are welders and people around them impacted by the work they do!!!!!!
Manganism or manganese poisoning is a toxic condition resulting from chronic exposure to manganese. It was first identified in 1837 by James Couper. Manganese superoxide dismutase (MnSOD) is the principal antioxidant enzyme in the mitochondria. Because mitochondria consume over 90% of the oxygen used by cells, they are especially vulnerable to oxidative stress. The superoxide radical is one of the reactive oxygen species produced in mitochondria during ATP synthesis. MnSOD catalyzes the conversion of superoxide radicals to hydrogen peroxide, which can be reduced to water by other antioxidant enzymes .
A number of manganese-activated enzymes play important roles in the metabolism of carbohydrates, amino acids, and cholesterol . Pyruvate carboxylase, a manganese-containing enzyme, and phosphoenolpyruvate carboxykinase (PEPCK), a manganese-activated enzyme, are critical in gluconeogenesis — the production of glucose from non-carbohydrate precursors. Arginase, another manganese-containing enzyme, is required by the liver for the urea cycle, a process that detoxifies ammonia generated during amino acid metabolism. So the doctors state: Magnesium
Supplemental magnesium (200 mg/day) has been shown to slightly decrease manganese bioavailability in healthy adults, either by decreasing manganese absorption or by increasing its excretion and motor disturbances, termed manganism. Generally, exposure to ambient manganese air concentrations in excess of 5 micrograms Mn/m3 can lead to Mn-induced symptoms.
In initial stages of manganism, neurological symptoms consist of reduced response speed, irritability, mood changes, and compulsive behaviors.[ Upon protracted exposure symptoms are more prominent and resemble those of idiopathic Parkinson’s disease, as which it is often misdiagnosed, although there are particular differences in both the symptoms (nature of tremors, for example), response to drugs such as levodopa, and affected portion of the basal ganglia. Symptoms are also similar to Lou Gehrig’s disease and multiple sclerosis.
This is caused by the inhalation of manganese fumes produced when working with carbon steel which cause serious side effects.
- Slurred speech
- Parkinson’s disease
- Impaired motor skills
- Poor co-ordination
- Difficulty with balance and walking
- Psychological problems
These symptoms affect the central nervous system and have a serious impact upon the affected person’s quality of life. But what constitutes a high level? As a trace element in people’s diet, manganese is essential to keeping organs, including the brain, healthy.
The American standard for the airborne concentration of manganese dust is now 5 milligrammes per cubic metre of air—a vast improvement on the doses of close to 1,000mg/m3 that some workers were exposed to only 60 years ago. Symptoms first appear after a chronic exposure of at least several months in duration:
1) Prodromal Phase: evidence of cognitive dysfunction and emotional disturbance begin to occur prior to severe motor and neurological dysfunction; symptoms may include fatigue, anorexia, muscle pain, nervousness, irritability, violent outbursts, insomnia, decreased libido, and labile affect; workers may also report headache, hypersomnia, spasms, weariness of the legs, and arthralgias;
2) Intermediate Phase: compulsive uncontrollable laughter or crying, clumsiness of movement, exaggeration of reflexes in lower limbs, speech disorders, visual hallucinations, excessive sweating, excessive salivation, and confusion;
3) Established Phase: muscular weakness, difficulty in walking, stiffness, impaired speech, mask-like face, increased muscular tone, slow and shuffling gait, micrographia, and resting tremors; the syndrome is indistinguishable from Parkinson’s disease;
Parkinsonism caused by manganese has the following that distinguish it from Parkinson’s disease: psychiatric symptoms early in the disease; cock walk; tendency to fall backward; less frequent resting tremor; more frequent dystonia; lack of response to dopaminomimetics; abnormal MRI showing manganese in the pallidum and caudate nucleus; and normal fluorodopa positron emission tomography scan. [IRRST] Characteristic findings of manganese poisoning are poor steadiness of hands, difficulty doing rapid alternating movements, muscular rigidity, and postural instability.
Entry of Mn to brain can occur via three known pathways: through the capillary endothelial cells of the blood–brain barrier, by the choroid plexus of the blood–CSF (cerebrospinal fluid) barrier, or via the olfac-tory nerve from the nasal cavity directly to brain. The latter is important, as most of the reported toxicities have occurred through the inhalation exposure. This review, however, will focus on the vascular routes, since contrast agents are routinely injected into the bloodstream.
The blood–brain barrier (BBB) lies in and around brain capillary cells and has physical, chemical and metabolic properties that influence movement of selected substrates. The capillary endothelial cells have tight junction proteins, which closely and securely link adjacent cells. The endothelial cells are surrounded by a basement membrane consisting of collagen and other lipophilic matrix proteins, which together slow the diffusion of water-soluble compounds. Astrocytes surround the capillary almost exclusively, covering an estimated 99% of the brain surface of the capillaries, leaving neurons to contact ≤ 1% of brain capillary surface. This connection of endothelial and glial cells with the basement membrane constitutes the physical BBB, which inhibits movement between the blood and brain. Substrates in blood may also be prevented from brain entry by their metabolism at the BBB. The barrier also contains transporter proteins whose distribution and activity influence movement across the BBB.