Effects on the lung health

When it comes to Al laser welding, the Al that ends up in the lungs comes mainly from welding fumes. The welding fumes consist largely of fine and ultrafine particles derived from the welded material and filler if it is used. The welding fumes contain very small particles of Al oxide. Welding gases typically also contain toxic gases such as ozone, nitrogen oxides, carbon dioxide and carbon monoxide. The use of shielding gases during welding reduces oxidation to some extent, resulting in less metal oxides in air. Secondly, the

use of a shielding gas can enhance ultraviolet radiation, thereby increasing the amount of photochemical gases, ozone and nitric oxide. Level of lung damage is affected by the amount of inhaled welding fumes and the dose, the exposure time, and the composition of the welding fumes and welding gases. Welders generally possess a wide variety of respiratory diseases.

These are the respiratory diseases commonly found in welders:

- Metal fume fever - Siderosis

- Pulmonary function abnormalities - Infectious pneumonia

- Fibrosis - Asthma

- Chronic bronchitis

- Chronic obstructive pulmonary disease - Lung cancer

(Riccelli et al. 2020, pp. 1-2, 9.)

Al fumes undeniably cause damage to lungs and respiratory system and lead to a wide variety of respiratory diseases, but the mechanism of Al-induced pulmonary toxicity is not yet fully understood. Al that has entered the lungs is currently thought to potentiate oxidative and inflammatory stress leading to lung epithelial dysfunction. Studies have found that smoking Al workers have a higher Al load than non-smoking Al workers (Elserougy et al. 2012, p.

76). It can be assessed that as the Al load to humans increases, health problems became worse after long period. Thus, some studies have found that smoking or non-smoking is not directly related to work ability or risk of getting sick (Li & Sung 1999, pp. 226-227).

Tobacco smoke contains quite a large number of Al, up to 0.37 % by weight, and more Al accumulates in lungs of smokers than in non-smokers. In one study for non-smoking Al workers the UAl (Urinary Al) is between 15.8 ± 4.6 mg/l and for smoking Al workers the UAl is between 20.5 ± 5.7 mg/l (Elserougy et al. 2012, p. 76). In addition to this lung study, it has been found that a decrease in C-reactive protein (CRP) levels and alpha-1 antitrypsin (A1AT) levels in the body are associated with an increase in Al levels and an increase in

respiratory problems. Monitoring of the A1AT level has appeared to be a promising way to prevent more advanced Al-induced lung diseases. Individuals with deficient A1AT levels should move away from jobs that cause Al exposure and thus prevent more serious respiratory problems at a later age. (Elserougy et al. 2012, pp. 73-77.)

A particular disease caused by Al in the lungs is called aluminosis. These kinds of diseases are generally called pneumoconiosis and they are caused by fine dust in the lungs containing Al, especially Al oxide. Studies have been found that Al particles with a size between 0.5 and 5 µm are the most dangerous for aluminosis (Guidotti 1975, pp. 16-17; Smolkova &

Nakladalova 2014, pp. 535-537). The first symptoms of aluminosis are dyspnoea on exertion and a dry cough. Aluminosis, if continued, leads to pulmonary fibrosis, where the lung surfaces scar and no longer function. The disease is serious, with deaths reported up to 3-5 years subsequent to the onset of symptoms. As with other pneumoconiosis, there is no effective treatment for aluminosis, and the resulting lung damage is permanent. Aluminosis is now a fully diagnosable and existing lung disease, although the pathophysiology of the disease has not been fully elucidated. Aluminosis has been observed most abundantly in persons working in the Al production involved with melting of bauxite, but also in abundance in those working with processing of fine Al powder and welding it. Aluminosis is currently a relatively rare disease, but due to the increasing use of Al, the risks leading to aluminosis must be considered and overcome. (Smolkova & Nakladalova 2014, pp. 535-537.)

The effects of Al fumes on the human respiratory system cause occupational asthma. Studies have been able to exclude the effects of general dust containing metal particles alone on the development of asthma, as no bronchial response was observed during mild steel welding, although the amount of respirable welding fumes has been significant (Vandenplas et al.

1998, pp. 1183-1184). A non-specific increase in bronchial hyperactivity has been observed with Al welding and such changes are frequently observed with asthmatic sensitivity. When comparing welding of steel to that of Al, it has been found that neither the fluorides in the welding gas nor the ozone created, neither chromium or nickel are expected to cause asthma symptoms. Moreover, the exact pathogens of work-related asthma are still unclear in welding, as the respirable welding gas contains such a wide variety of metal particles as well as a variety of gases and fumes. The IgE (Immunoglobulin E) -mediated mechanism of a

specific antibody against allergic reactions in the body is thought to be involved in the pathogens of Al-induced asthma. A specific Al-induced asthma, called potroom asthma, is a disease observed in primary Al production workers as well as Al salt production workers, and Al welders are assumed to possess similar susceptibility and disease mechanisms to occupational asthma. (Vandenplas et al. 1998, pp. 1182-1184.)