Cause:An acquired porphyria due to elemental Pb ingestion; paint ingestion esp in children (Nejm 1974;290:245), battery fumes, moonshine (Nejm 1969;280:1199), pottery glazes commercial and homemade (Nejm 1970;283:669), air contamination from smelter (Nejm 1975;292:123), indoor firing range users (Am J Pub Hlth 1989;79:1029), and radiator repair mechanics (Nejm 1987;317:214). Tetraethyl Pb from gas results in encephalopathy, without porphyria or blood changes

Pathophys:Pb inhibits by chelating sulfhydryl (SH) groups of ALA dehydrogenase (ALA PBG), ferrochelatase (PP heme), and possibly ALA synthetase. In adults, gout and gouty nephropathy; latter always associated with overt or silent Pb intoxication (Nejm 1981;304:520)

Common in young children; adult exposures usually occupational, eg rehab'ing old buildings. Inversely correlated w vit C intake (Jama 1999;281:2289)

Sx:In severe poisoning, abdominal colic, relieved by palpation! h/o family pet illness, eg, dog (Am J Pub Hlth 1990;80:1183)

Si:In severe poisoning, anemia, gingival margin lead line, motor peripheral neuropathy, eg, wrist drop, neuroses, and psychoses

Progressive, si and sx roughly correlate w blood lead levels; cognition deficits only partially reverse w long-term rx (Jama 1998;280:1915)

• Antisocial/delinquent behaviors long term (Jama 1996;275:363)
• Renal impairment (Ann IM 1999;130:7; Jama 1996;275:1177)
• Gout and gouty nephropathy
• Encephalopathy—mortality without rx is 50%, with rx is 3%
• Mental deficiencies and neurologic abnormalities even at blood levels <50 µgm % (Nejm 1988;319:468) and long term in children with elevated Pb in teeth representing old exposure (Nejm 1990;322:83) or with umbilical cord Pb levels 10 µgm/mL (Nejm 1987;316:1037). Measurable behavioral problems at levels 15-50 µgm % (Am J Pub Hlth 1992;82:1356); before age 3, eventual IQ impaired even at average blood levels <10 µgm % (Nejm 1992;327:1279)
• Hypertension, "essential hypertensives" with creatinine >1.5 mg % often are really lead toxic (Jama 2003;289:1523; 1996;275:1171; Am J Pub Hlth 1999;89:330)
• Dental caries (Jama 1999;281:2294)

Lab:

Chem:Whole blood lead levels, even levels of 5-6 µgm % may indicate chronic lead load and may benefit from rx if creatinine >1.5 mg % (Nejm 2003;348:277); tooth levels (deciduum) can be used for epidemiologic studies (Nejm 1974;290:245)

Hem:Rbc stippling (RNA and mitochondria), siderocytes. Free erythrocyte protoporphyrin no longer used as screening test because only sensitive down to 30-40 µgm % and levels lag weeks

Urine:Increased coproporphyrins and protoporphyrins, no PBG elevations; Pb levels elevated; EDTA mobilization tests

Xray:KUB may show Pb opacities in gut; bones show lead lines at metaphyseal calcification line in children due to increased calcium laid down at zone of provisional calcification in rapidly growing bones, not in adults

Rx:

Primary prevention by decreasing exposures is best health policy since now even levels <10 are shown to significantly effect IQ of children (Nejm 2003;348:1515, 1517, 1527)

Screen all children with serum lead levels at 6-12 mo and q6-12mo to age 24 mo, screen older children only if high risk (Med Let 1991;33:78) (Table 1.2)

Table 1.2 Lead Poisoning Protocol

Chelation w (none have been shown to improve neurologic function aside from seizures)

• Succimer (DMSA, dimercaptosuccinate) po (Jama 1991;265:1802) if no gi toxicity or encephalopathy, or
• BAL (dimercaprol) im if level >100 µgm/mL and or sx; contraindicated in peanut allergy; followed not sooner than 4 h (to avoid encephalopathy) by
• EDTA iv 1 gm weekly, does abort nephropathy (Nejm 2003:348:277)
• Vitamin C perhaps (Jama 1999;281:2289, 2340)