Low-Level Lead Exposure & Implications for Human Health

In 2017, lead exposure accounted for 1.06 million deaths and 24.4 million years of healthy life lost worldwide.¹ The highest burden was in low- and middle-income countries. The Institute for Health Metrics and Evaluation also estimated that in 2016, lead exposure accounted for 63.2% of the global burden of idiopathic developmental intellectual disability, 10.3% of the global burden of hypertensive heart disease, 5.6% of the global burden of ischemic heart disease, and 6.2% of the global burden of stroke.¹

In adults, sufficient evidence suggests that blood lead levels (BLLs) <5 ?g/dL are associated with decreased renal function and that BLLs <10 ?g/dL are associated with increased blood pressure and hypertension.²

Lead is one of the most widely used metals in the world,³ and although it is toxic, it has been incorporated into many different products, including paints, cosmetics, fuel, etc., for its unique properties like a low melting point and resistance to corrosion.⁴ However, lead persists in the environment and cannot be metabolized in the human body.³ It can enter the body via a variety of routes; e.g., particles from lead-based paint or housing renovation can adhere to food and be ingested, and industries that use lead in manufacturing can pollute the air and soil, exposing humans via the food chain.⁵

An interesting study in 2019 looked at differing sources of lead exposure in various countries. Sources include:

Lead can be absorbed by the intestine and through the skin, and almost 90% of it binds to erythrocyte proteins.⁴ Once inside the human body, lead may travel to different tissues and organs, including the liver and kidneys, where it can cause oxidative damage to cells and tissues, including uncoupling the respiratory chain in mitochondria.⁴ DNA damage is a significant consequence of oxidative stress.³

A 2018 study provided the first published evidence that lead exposure results in DNA damage via promoting oxidative stress and promoter methylation of DNA repair genes in human lymphoblastoid TK6 cells.³ This study was carried out on only one human cell line, whereas the obtained results need to be verified in multiple human cell lines, and the role of DNA repair proteins in lead-induced genotoxicity is unclear and needs further elucidation. Taken together, however, the study results indicate that lead exposure decreased cell viability, induced oxidative stress–mediated DNA damage via the Nrf2-ARE signaling pathway, and decreased the expression of DNA repair genes.³