Occupational Physician

A case I just saw, quite impressive from a medical point of view:

A 35-year old man presented with abdominal colicative pain with acute onset, at his workplace, one hour after starting the night shift. At hospital presentation, about 30 hours later, the pain not only persisted but increased in intensity and symptoms also included nausea, vomiting, loss of appetite or intestinal transit in the last few days.

He has been working for only two months as a foundry worker in the (primary) smelting industry of raw lead ore, in the most polluted town in Europe, Copsa Mica, Sibiu county, Romania. At his workplace, he was was exposed to molten metal fumes (lead and zinc), of high concentration. He said he was given a respirator and the filters/cartridges were changed every few days.

Physical examination was little remarkable: except for epigastric and periombilical pain, Burton’s line (a black line on the gums) and an antialgic body posture, there were no other signs.

As weird as it sounds, in this occupational medicine clinic there is no way to perform atomic absorption spectrophotometry which provides accurate quantitative analyzes for blood lead, so the lab diagnostic use to be based only on urinary lead excretion as indicator of exposure. However, the laboratory technician is in vacation, so not even this analysis could be performed. Urinary delta-aminolevulinic acid, ALA-U, [>25 mg/l] and coproporphyrins, CP-U [1230 ug/l] used as indicators of biological effect were well above normal values, therefore indicating a string inhibition of heme synthesis.

Laboratory findings also showed anemia [hemoglobin 10,6 g/dl] due to increased erythrocyte destruction [urinary urobilinogen 30mg/l, urinary bilirubin 3mg/l]. Other findings: microproteinuria [initially 30mg/l, a few days later 100mg/l]. All other analysis were within normal limits.

The textbook says that lead-induced hemolysis is caused by increased membrane fragility produced by the inhibition of sodium/potassium adenosine triphosphatase and pyrimidine 5′-nucleotidase.

This inhibition of pyrimidine 5′-nucleotidase also impairs elimination of degrading RNA, which can manifest as basophilic stippling of erythrocites. And this patient does have basophilic stippling…

He was given chlorpromazine 25 mg bid im [commercial product Plegomazin] which controlled well the saturnine colic, but also induced sleeping, which was actually quite a good idea, given patient’s initial state of exhaustion. He underwent chelation therapy with d-penicillamine 250 mg po qid [commercial product Cuprenil], the only currently chelator available in Romania [EDTA used to be the first choice, but its production has been discontinued in Romania, for it being too cheap to produce and commercially uneffective.

The clinical evolution is favorable, the patient became completely asymptomatic within a few days, just that today, 8 days after ingression his ALA-U level is still 23.5 mg/l [normal range u to 10mg/l]. This indicates a massive inhibition of heme synthesis enzymes, due to massive exposure and absorption of lead.

But then what? He’ll probably return to his workplace, even against medical advise, hopefully moved to a workstation with lower exposure, just to become intoxicated again and again over the years and watch his health deteriorating. Some of his work colleagues were already intoxicated 20 times… But more on the chronic lead intoxication in another post.