Genotoxic Effect of Lead and Cadmium on Workers at Wastewater Plant in Iraq

Abstract

Heavy metal poisoning is a worldwide problem that is caused by different human industrial activities such as battery and painting manufacturing and occupational exposure of those working at petrol stations. Wastewater is known to contain higher amounts of heavy metals such as lead (Pd) and cadmium (Cd) and might be sources of exposure for workers at the wastewater treatment plant. However, to our best knowledge, no studies were done to evaluate the level of cadmium and lead in blood of workers at wastewater treatment plants and evaluate the subsequent effect of lead and cadmium on delta-aminolevulinic acid dehydratase (δ-ALAD), urinary delta-aminolevulinic acid (Uδ-ALA), and 8-hydroxy-2′-deoxyguanosine (8-OHdG) as markers of lead and cadmium toxicity. In this case-control study, 79 workers at the Al-Rustumiya wastewater plant in Baghdad, Iraq, and 40 control subjects were included. The levels of lead and cadmium were measured in blood of the study subjects using the atomic absorption spectroscopy (AAS) method. 8-OHdG was analysed using enzyme-linked immunosorbent assay (ELISA) technique. δ-ALAD and Uδ-ALA were estimated using spectrophotometry-based methods. Our work showed that workers had a significantly higher level of lead and cadmium when compared with the control group (P<0.05), yet, still within the World Health Organization permissible limit. The level of both metals was positively associated with duration of work at the plant (P<0.01). The activity of δ-ALAD was inversely associated with the lead level, while both Uδ-ALA and 8-OHdG were positively correlated with the lead level (P<0.05). These three markers lacked any statistically significant association with the cadmium level (P>0.05). To sum up, working at the wastewater treatment plant was associated with a higher blood level of lead and cadmium and their possible health hazard. Health and occupational safety authorities are required to set up tighter regulations and protocols to minimize these hazards and ensure a safe working environment.

Genotoxic Effects of Lead and Their Impact on the Expression of DNA Repair Genes

“…The International Agency for Research on Cancer (IARC) has classified Pb as a possible human carcinogen (group 2B) and its inorganic compounds as probable human carcinogens (group 2A). The genotoxic effects of Pb have been investigated for many years and include chromosome aberration (CA), mutation, DNA breakage, and DNA synthesis inhibition [ 14 , 15 ]. According to previous studies, the end-points of the genotoxic effects of Pb have been well-demonstrated in different in vitro, in vivo, and epidemiological studies.…”

“…8-OHdG is one of the predominant forms of oxidative lesions and has been widely used as a biomarker for oxidative stress [ 26 ]. Several studies demonstrated a positive relation between 8-OHdG and Pb [ 15 , 27 , 28 ]. The DNA repair machinery plays the crucial role of protecting the cells from DNA damage generated by exposure to carcinogens and cytotoxic agents, as well as heavy metals.…”

Metabolic and genetic derangement: a review of mechanisms involved in arsenic and lead toxicity and genotoxicity

“…By inhibiting δ-aminolevulinic acid dehydratase, Pb favours the accumulation of ALA, which triggers ROS production, but also acts as a carcinogen (116). ALA-mediated oxidative DNA damage occurs through the production of 8-OHdG, 8-hydroxyguanine (8-oxo-7,8-dihydroguanine), and 8-oxo-7,8-dihydro-2deoxyguanosine (8-oxodG) (116,152). A number of studies has reported positive correlation between ALA levels and markers of oxidative stress and carcinogenesis (116,137,141,153).…”

“…ALA-mediated oxidative DNA damage occurs through the production of 8-OHdG, 8-hydroxyguanine (8-oxo-7,8-dihydroguanine), and 8-oxo-7,8-dihydro-2deoxyguanosine (8-oxodG) (116,152). A number of studies has reported positive correlation between ALA levels and markers of oxidative stress and carcinogenesis (116,137,141,153). Furthermore, hydroxyl radicals (HO•) generated by ALA attack DNA strands and interact with its nucleobases to produce various oxidation products.…”

“…The 8-oxodG lesion (HO• interaction with guanine) is the most abundant and is promutagenic (141). Unrepaired 8-oxodG can lead to genomic instability through transversions and the formation of double-strand breaks (116,154). Furthermore, several studies (155)(156)(157) have revealed the epigenetic function of 8-oxodG, and its role in carcinogenesis through gene regulation.…”