Effect of occupational exposure to lead on serum levels of lipid profile and liver enzymes: An occupational cohort study

Firoozichahak, Ali; Rahimnejad, Samira; Rahmani, Abdolrasoul; Parvizimehr, Ali; Aghaei, Abbas; Rahimpoor, Razzagh

doi:10.1016/j.toxrep.2022.02.009

Cited by 24 publications

(24 citation statements)

References 37 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The fields around the welders (breathing zone) contain the contaminants produced during welding operations 21 . Lead is one of these pollutants, and 40% of inhaled lead is absorbed to blood circulation, which is the main rout of inorganic lead absorption 6,22 . in the present study, we have investigated the ALCs and BLCs of automobile welders in Birjand city.…”

Section: Discussionmentioning

confidence: 99%

“…Respiratory and gastrointestinal tracts are the main routs of inorganic lead absorption, so workers’ exposure to lead mainly occur through the respiratory tract (40% of inhaled lead is absorbed into the blood plasma). The circulating lead is bound to erythrocytes for about 30 days, and is therefore distributed in several organs, such as the kidneys, liver, brain, bones, teeth, etc 6 . After exposure, the half-life of lead elimination from blood would be about 30 days, but it remains in bones for 10-20 years; So, BLC could be considered as an indicator for recent lead exposure 7 .…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

An Investigation of Lead Concentration in the Breathing Air and the Blood of Automobile Welders in Birjand, Iran

Motamedrezaei

Gholami

Sharifzadeh

et al. 2022

Preprint

View full text Add to dashboard Cite

Introduction: Lead is known as one of the most dangerous toxic metals in the world and its entry into the body can cause acute and chronic intoxication with a wide range of systemic symptoms. Our goal in the current research is to study the level of lead in the breathing zone and blood of the automobile welders in Birjand. Methods: A cross-sectional, descriptive-analytic study was conducted on 47 automobile welders. The criteria for entering the study included, male gender, having at least 1 year of experience in automobile welding, and at least 8 hours of daily employment in welding. The general information required was collected through a questionnaire. At the beginning of the study, in each working environment air samples were taken in accordance with NIOSH 7082 standards. The analysis of the air lead concentration (ALC) was carried out by a flame atomic absorption spectrophotometer. The blood lead concentration (BLC) was measured by NIOSH 8003 method via graphite furnace atomic absorption spectrophotometer. Results: Based on the data, 12.8% of the workers were smokers and 66% used appropriate personal protective equipment. The average ALC was 0.0458 +/- 0.0296 mg/m3 and the average BLC of automobile welders was 9.89 +/- 7.32 μg/dL. Although Pearson correlation coefficient showed a positive correlation between ALCs and BLCs, this correlation was not statistically significant (p = 0.38, r = 0.18). Conclusion: The findings of this study showed that the average BLC in cigarette smokers and those who did not use PPE was higher than other people; besides, it was higher in individuals over the age of 30 than those under this age. The mean BLC in automobile welders and the mean ALC corresponded to the standards of the American Conference of Governmental Industrial Hygienists (ACGIH).

show abstract

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

An Investigation of Lead Concentration in the Breathing Air and the Blood of Automobile Welders in Birjand, Iran

Motamedrezaei

Gholami

Sharifzadeh

et al. 2022

Preprint

View full text Add to dashboard Cite

show abstract

“…Lead (Pb for Latin plumbum) overdose in animals caused experimental liver injury. Elucidating its pathogenic background was challenging as some issues remain controversial, although many studies have been published [ 63 , 64 , 65 , 66 , 67 , 68 , 69 , 70 , 71 , 72 , 73 ]. Consensus exists among experts that ROS as a product of oxidative stress plays a major role in initiating the injury process [ 12 , 63 , 64 , 65 , 66 , 67 , 68 , 69 ].…”

Section: Leadmentioning

confidence: 99%

“…Elucidating its pathogenic background was challenging as some issues remain controversial, although many studies have been published [ 63 , 64 , 65 , 66 , 67 , 68 , 69 , 70 , 71 , 72 , 73 ]. Consensus exists among experts that ROS as a product of oxidative stress plays a major role in initiating the injury process [ 12 , 63 , 64 , 65 , 66 , 67 , 68 , 69 ]. Pb binds to sulfhydryl groups of structural proteins or any cytosolic protein such as glutathione, thereby reducing the antioxidant defense property and enhancing the Pb toxicity [ 64 , 65 , 67 , 68 , 70 , 71 ] through lipid peroxidation of cell membranes, such as of mitochondria or endoplasmic reticulum [ 12 , 64 , 65 , 66 , 70 , 72 ].…”

Section: Leadmentioning

confidence: 99%

“…Consensus exists among experts that ROS as a product of oxidative stress plays a major role in initiating the injury process [ 12 , 63 , 64 , 65 , 66 , 67 , 68 , 69 ]. Pb binds to sulfhydryl groups of structural proteins or any cytosolic protein such as glutathione, thereby reducing the antioxidant defense property and enhancing the Pb toxicity [ 64 , 65 , 67 , 68 , 70 , 71 ] through lipid peroxidation of cell membranes, such as of mitochondria or endoplasmic reticulum [ 12 , 64 , 65 , 66 , 70 , 72 ]. The high affinity of Pb to protein sulfhydryl groups resulted in lower activities of a number of enzymes like catalase, glutathione peroxidase, glucose-6-phosphate dehydrogenase, and superoxide dismutase [ 65 , 72 ].…”

Section: Leadmentioning

confidence: 99%

See 1 more Smart Citation

Aluminum, Arsenic, Beryllium, Cadmium, Chromium, Cobalt, Copper, Iron, Lead, Mercury, Molybdenum, Nickel, Platinum, Thallium, Titanium, Vanadium, and Zinc: Molecular Aspects in Experimental Liver Injury

Teschke

2022

IJMS

View full text Add to dashboard Cite

Experimental liver injury with hepatocelluar necrosis and abnormal liver tests is caused by exposure to heavy metals (HMs) like aluminum, arsenic, beryllium, cadmium, chromium, cobalt, copper, iron, lead, mercury, molybdenum, nickel, platinum, thallium, titanium, vanadium, and zinc. As pollutants, HMs disturb the ecosystem, and as these substances are toxic, they may affect the health of humans and animals. HMs are not biodegradable and may be deposited preferentially in the liver. The use of animal models can help identify molecular and mechanistic steps leading to the injury. HMs commonly initiate hepatocellular overproduction of ROS (reactive oxygen species) due to oxidative stress, resulting in covalent binding of radicals to macromolecular proteins or lipids existing in membranes of subcellular organelles. Liver injury is facilitated by iron via the Fenton reaction, providing ROS, and is triggered if protective antioxidant systems are exhausted. Ferroptosis syn pyroptosis was recently introduced as mechanistic concept in explanations of nickel (Ni) liver injury. NiCl2 causes increased iron deposition in the liver, upregulation of cyclooxygenase 2 (COX-2) protein and mRNA expression levels, downregulation of glutathione eroxidase 4 (GPX4), ferritin heavy chain 1 (FTH1), nuclear receptor coactivator 4 (NCOA4) protein, and mRNA expression levels. Nickel may cause hepatic injury through mitochondrial damage and ferroptosis, defined as mechanism of iron-dependent cell death, similar to glutamate-induced excitotoxicity but likely distinct from apoptosis, necrosis, and autophagy. Under discussion were additional mechanistic concepts of hepatocellular uptake and biliary excretion of mercury in exposed animals. For instance, the organic anion transporter 3 (Oat3) and the multidrug resistance-associated protein 2 (Mrp2) were involved in the hepatic handling of mercury. Mercury treatment modified the expression of Mrp2 and Oat3 as assessed by immunoblotting, partially explaining its impaired biliary excretion. Concomitantly, a decrease in Oat3 abundance in the hepatocyte plasma membranes was observed that limits the hepatic uptake of mercury ions. Most importantly and shown for the first time in liver injury caused by HMs, titanium changed the diversity of gut microbiota and modified their metabolic functions, leading to increased generation of lipopolysaccharides (LPS). As endotoxins, LPS may trigger and perpetuate the liver injury at the level of gut-liver. In sum, mechanistic and molecular steps of experimental liver injury due to HM administration are complex, with ROS as the key promotional compound. However, additional concepts such as iron used in the Fenton reaction, ferroptosis, modification of transporter systems, and endotoxins derived from diversity of intestinal bacteria at the gut-liver level merit further consideration.

show abstract

Environmental toxicant-mediated cardiovascular diseases: an insight into the mechanism and possible preventive strategy

Asiwe,

Oritsemuelebi

2023

Toxicol. Environ. Health Sci.

View full text Add to dashboard Cite

Effect of occupational exposure to lead on serum levels of lipid profile and liver enzymes: An occupational cohort study

Cited by 24 publications

References 37 publications

An Investigation of Lead Concentration in the Breathing Air and the Blood of Automobile Welders in Birjand, Iran

An Investigation of Lead Concentration in the Breathing Air and the Blood of Automobile Welders in Birjand, Iran

Aluminum, Arsenic, Beryllium, Cadmium, Chromium, Cobalt, Copper, Iron, Lead, Mercury, Molybdenum, Nickel, Platinum, Thallium, Titanium, Vanadium, and Zinc: Molecular Aspects in Experimental Liver Injury

Environmental toxicant-mediated cardiovascular diseases: an insight into the mechanism and possible preventive strategy

Contact Info

Product

Resources

About