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ON AUGUST 17, 1913, a five-year-old child in Baltimore’s Home of the Friendless complained about a pain in his face and head. He slept poorly and appeared ill. The following morning his condition worsened, and he developed a stiff neck and seizures before lapsing into coma. These distressing symptoms prompted his transfer to Johns Hopkins’s children’s hospital, the Harriet Lane Home. There his doctors, Henry M. Thomas and Kenneth D. Blackfan, initially believed that he suffered from a severe infection of the central nervous system. To their surprise, tests for meningitis—bacterial and tubercular—and neuro-syphilis were repeatedly unrewarding. As Thomas and Blackfan observed their young patient over the next few days, they noted additional distressing problems. His left eye turned inward, his right optic nerve was swollen, and his retinas displayed hemorrhages. Despite these troubling symptoms and the frustration of not having a diagnosis, the boy improved so that a week later he was “nearly well.” Able to speak, he complained of a stomachache and headache. After a month in the Harriet Lane Home, he returned to the Home of the Friendless, restored to health but still an enigma.
He remained healthy for six months, until March 1914. Then he suddenly complained of headache and vomiting, developed seizures, and once again lapsed into coma. The boy was quickly transferred to the Harriet Lane Home, where the same doctors once more suspected an infection of the central nervous system and once more were unable to prove it. A diagnostic dilemma brought the boy’s condition into sharp scrutiny. On one exam, a doctor noted that there was a faint bluish discoloration in the gum around one tooth. This unlocked the puzzle, because physicians were accustomed to seeing similar markings in factory workers who inhaled or swallowed too much lead on the job. Physicians at Johns Hopkins had not considered lead poisoning in the boy because it was not reckoned a problem for children, unless they worked as a painter’s apprentice or in a lead-manufacturing plant.
Once the diagnosis was suspected, Thomas and Blackfan puzzled over the source of lead, because this boy was neither an apprentice nor a child laborer. During the course of his hospitalization, they found his mouth filled with paint flakes that he had gnawed off his hospital crib. On visiting his bed at the Home of the Friendless, they noted that he had also chewed paint from his furniture there. Alerted to his habit, nurses noted that “he would gnaw any painted object unless he was most carefully watched.”
The boy recovered and returned to the Home of the Friendless in early May. Three weeks later he developed seizures once more. He died before he could be sent back to the Harriet Lane Home.1
One year later, a two-year-old boy with seizures came to the Harriet Lane Home. Blackfan, schooled from the earlier case, looked closely at the toddler’s gums and found a similar blue line. He still checked for infection, for in 1915 this was by far the most common cause of seizures in a young child. In this twoyear- old, Blackfan also noted an abnormality in the red blood cells—stippling— a diagnostic aid used in factory workers suspected of lead poisoning. The boy was discharged after two weeks. Unfortunately, just one day later, he seized again, and died shortly after being rushed back to the Harriet Lane Home. Blackfan asked the boy’s father about a source of lead and learned “that the child would gnaw any painted article, and that he and his brother had recently ruined a set of parlor furniture by eating paint from it.”2 Six months later, his fraternal coconspirator, now just two years old, also developed seizures. Of note, Blackfan found that around the time of his brother’s death the boy had suffered from abdominal pains so severe that a surgeon operated for suspected appendicitis. At surgery, the appendix was not inflamed, and the surgeon was perplexed about the cause of the abdominal distress. Blackfan surmised that unsuspected lead poisoning had been the culprit. Blackfan attempted to control the boy’s seizures; despite enormous efforts, this toddler also died.
At the end of July 1915 another boy, three years of age, came to the Harriet Lane Home with seizures and coma. He had a blue line on his gums. The boy improved in the hospital, but once he awoke from his coma, he displayed a paralysis of his facial muscles. Fortunately, this child survived. Blackfan was unable to determine his source of lead.
Not only were these four boys the first children that Blackfan had encountered with lead poisoning, but the three who died were the first reported American cases of toddlers poisoned from gnawing paint from cribs or other furniture Children and Lead 9
at home. Lead poisoning was not a new disease in the second decade of the twentieth century, but when it occurred it did so in environments very different from the surroundings of these infants. Lead poisoning was a disease of workers employed in one of the many lead trades. Physicians therefore normally thought of lead poisoning as a disease of adults.
Over the course of the nineteenth century, physicians and workers came to appreciate the large number of telltale signs and symptoms of lead poisoning or “plumbism” on the job. Most common were abdominal cramps, or colic, which could incapacitate workers. Particularly distressing was numbness or even paralysis of fingers, hands, wrists, toes, feet, and ankles, complaints that went by the terms foot-drop, wrist-drop, or peripheral neuropathy (because the symptoms demonstrated injury to peripheral nerves). Lead in greater amounts damaged the brain or central nervous system, resulting in seizures, coma, and even death. Many lead workers had a light blue line on the gums above the teeth, which was the product of lead and poor oral hygiene. Many were pale from anemia.3 In addition to adults, a few children in the nineteenth century, and to a lesser extent in the twentieth century, also worked in lead industries, thus providing physicians with some information about how children experienced lead poisoning. Industrial hygiene was thus a logical place for Blackfan to turn in search of insights. What he found was an occupational disease so different from the one his young patients suffered that it offered few helpful guides. For example, Blackfan recognized that most lead workers were poisoned through inhaling the clouds of dust that swirled around the workplace. This environment did not occur in the homes of Baltimore’s infants. In contrast, Blackfan’s patients chewed and swallowed far smaller amounts of lead.4
At the time that Thomas and Blackfan observed their cases, there were foreign examples of children who had developed lead poisoning at home. Children in Queensland, a remote and tropical region of northern Australia, had suffered from household lead poisoning, and Thomas and Blackfan’s published papers give evidence that they explored the outlines of this Australian epidemic. What Thomas and Blackfan discovered was a disease that differed in symptoms, in age of victims, and in contexts from the disease that their patients experienced in Baltimore.
In addition, Blackfan knew that there were a few cases of American children lead-poisoned in their homes. These afflicted children also provided limited insights, because they had ingested the metal in ways and in circumstances considerably different from those of the children whom Blackfan and Thomas treated at the Harriet Lane Home. Consequently pediatricians in the United States had to develop an entirely new way to conceptualize the domestic hazard of lead. This view shaped public health efforts until the late 1940s.
Domestic Lead Poisoning in Children
For information about household lead poisoning, American pediatricians could read about the experiences of a small number of children which revealed that lead paint was an uncommon source of lead at the time that Blackfan encountered his cases in 1914–1917. In particular, Blackfan turned to an epidemic of lead poisoning suffered by children and adults in Philadelphia following the ingestion of pastry buns that had been dyed with a food coloring made from lead chromate. This epidemic was recent and numerically significant. Even more important to Blackfan, the victims of bun poisoning had seizures, the symptom he was seeing in Baltimore’s children after gnawing paint from cribs. In 1887 David Stewart investigated the home of a Philadelphian family of nine who had been struck—sequentially—with vomiting, headaches, and seizures. Four children died. Dr. Stewart suspected lead poisoning from the blue gum lines that several victims had. Stewart made a home visit, investigating the usual sources of lead: water pipes, pottery glazes, linings of “iron” pots. None contained lead. On questioning the family about possible food contamination, Dr. Stewart learned that they shopped at a new bakery. A visit to the bakery revealed that a member of the baker’s family had also died of convulsions. On questioning the baker, Dr. Stewart determined that the baker had used chromium yellow (lead chromate) as a substitute for egg yolk to produce more enticing yellow pastries.5 Two years later a physician in Baltimore, William Glenn, reviewed the medical literature and found over one hundred cases of lead poisoning caused by the use of lead pigments as food colorings. Following Stewart’s example, Glenn investigated Baltimore bakeries, but he discovered none using the dangerous substitutes. He did, however, find lead chromate in candies sold at street fairs.6 In 1895 Stewart reported sixteen additional cases with seizures in Philadelphia. Once again, several cases occurred in the home of a baker.7 Two features made these patients noteworthy: the source of lead and the seizures. Stewart informed his readers that L. Tanquerel des Planches, a renowned French industrial hygienist of the mid-nineteenth century, had claimed that lead encephalopathy was the rarest problem he encountered in a career devoted to industrial lead poisoning. For Stewart, seizures were the most common complaint.