The tests used were haemoglobin, reticulocyte count, and blood lead, and urinary lead, coproporphyrin, δ-aminolaevulinic acid (ALA), and porphobilinogen (PBG) estimations. Of these, the urinary lead was similar for all three groups and the blood lead estimation was of less value for determining the clinical group of the men than the haemoglobin and urinary coproporphyrin or ALA estimations, which correlated well with the clinical assessment and with each other but showed no correlation with the urinary and blood lead levels. PBG levels became raised only with the onset of symptoms of lead poisoning.

A haemoglobin of 13 g./100 ml. (90%) or less is a cautionary sign. Urinary coproporphyrin above 80 μg./100 mg. creatinine (800 μg./litre), ALA above 2·0 mg./100 mg. creatinine (2·0 mg.%), and PBG above 0·15 mg./100 mg. creatinine (0·15 mg.%) were almost always associated with symptoms or signs and were therefore considered to be the upper safety limits. Although the blood lead level does not differentiate between lead toxicity and lead exposure, values above 60 μg. lead/100 g. blood should alert the physician to carry out other tests.

In addition to the above tests, blood pressure, blood urea, and serum uric acid estimations were performed on all the men in order to elucidate the possible role of lead in the production of renal damage. Blood pressure and serum uric acid levels were similar for all three groups but the blood urea level was raised in group C. The reason for this finding was not established.

It was found that scrap metal burning, battery manufacturing, and ship-breaking constituted the gravest lead hazards encountered in this survey whereas wire manufacture constituted the least. Workers in the most modern factory, a car-body pressing plant, gave average values just below the danger levels for the urinary coproporphyrin and ALA estimations despite apparently efficient protective measures. This finding underlines the importance of the medical supervision of lead workers.