The Haemopoietic system was one of the earliest principal targets of lead (Pb) to be recognized and intensely studied but largely from temperate developed countries. This study reports investigations into the haemotobiochemical variations associated with occupational Pb poisoning in a tropical developing country.
One hundred and thirty seven (137) subjects comprising 86 lead workers and 51 appropriately matched controls were studied. The lead workers all males included battery workers, home and autopainters, automechanics, welders, gasoline dispensers and ceramic workers. They were classified according to exposure categories based on the prevailing air lead level (PbA) at the occupational environment.
Blood lead (PbB) was significantly higher in lead workers than in controls (P<0.001). the PbB of controls (occupationally unexposed) was also significantly higher than in communities that have either reduced or eliminated lead from petrol. Erythrocyte protoporphyrin (EPP) and prophobilinogen (PBG) were similar in lead workers and controls. The haem degradative product bilirubin was unlike EPP and PBG higher in controls (P<0.05). Indices of iron (Fe) homeostasis, serum Fe, total iron binding capacity (TIBC), transferrin, and percentage Fe saturation did not differ between lead workers and control (P>0.05) in all cases. There was also no alteration in RNA inetabolism as indicated by the absence of basophilic stippling in the erythrocytes of lead workers. Some indices of erythropoietic activity Hb, PCV and MCHC were all significantly decreased in lead workers, compared with controls (P<0.001) in all cases. In contrast, the haem cofactor metals, copper (Cu) and zinc (Zn) levels were significantly elevated in lead workers compared with controls (P<0.01; P<0.001) respectively. There was no variation with exposure category.
These complex observations may suggest the interplay of acute phase and antioxidant responses of Cu in caeruloplasmin and Copper-Zinc supper oxide dismutase (Cu-Zn SOD) as well as the inhilation ('supplementation') of Zn fume from the occupational environment. This synergy appears to have significantly restored the activity of the major haem pathway enzyme, d-aminolaevulinate dyhydratase (ALA-D) a Zn dependent enzyme that is exquisitely inhibited by Pb. Thus modulating the deleterious effect of Pb on the haemopoietic system.
These observations imply that the combination of the well known Zn deficiency in many tropical countries and the substantial environmental lead pollution may predispose the general population to a significantly depressed haemopoietic system. This may in turn increase the prevalence of subclinical or oven anaemia of 'uncertain' aetiology in the presence of other haem pathway stressors such as malnutrition.
