Recently in Medical history Category
A lot more obscure than the "seven-fourteen" slang for Quaalude, "420," as a code for Mary Jane, is exhaustively mined by Ryan Grim of the HuffPo. (And God help me, I'm linking to the HuffPo).
HT: KPB, my (what else) college roommate.
Photo of growing marijuana plant from the Department of Justice.
King Tut was buried in his condo made of stone-a after succumbing to the severest form of malaria, malaria tropica, say preeminent medical archaeologists in this week's JAMA. The boy king also had a form of osteochondrosis—namely, avascular necrosis of the second and third metatarsal bones (in the foot). The bone disease, which probably caused limping, explains the afterlife canes placed in Tut's tomb.
The conclusions about Tut's medical problems were made on the basis of an unprecedented combination of anthropologic, genetic, and radiologic studies and free access to the mummified remains of Tut and those of other Egyptian royalty. The researchers propose that the immediate cause of Tut's death was likely a leg fracture (possibly from a fall), which precipitated a series of life-threatening events in the already medically compromised teenager.
Crashing the curiosity party, U Michigan's Howard Markel raises the sticky issue of ethics when conducting medical examinations on historical subjects in an accompanying JAMA editorial. "Are major historical figures entitled to the same privacy rules that private citizens enjoy even after death?" he asks. While Markel acknowledges, "All historians are guilty of enjoying reading the mail and personal materials of others," he advises,
[B]efore disturbing the dead with the penetrating wonders of 21st-century medical science, it is essential to follow the lead of these authors by pondering all the ethical implications of such inquiries to avoid opening a historical Pandora's box.
Steve Martin, who wrote that Tut "gave his life for tourism," would probably concur.
Photo of banner advertising the 2008 tour of Tut's tomb artifacts from http://www.atlantaga.gov/media/citynewsbytes_040808.aspx.
While film director Roman Polanski fights extradition to the United States, time is taken here to remember Quaalude—the drug that a 43-year-old Polanski allegedly gave to a 13-year-old girl before he had sex with her in 1977.*
Quaalude is the trade name for methaqualone, a chemical developed in the 1950s in India as an antimalarial compound. Contemporaneous data also indicated that the drug provided "good hypnotic activity" and had "low toxicity" when compared with widely used barbiturate sedatives. Consequently, during the 1960s, the drug became a popular prescription alternative to potentially addictive agents like secobarbital (Seconal; Eli Lilly) for the treatment of insomnia.
In the United States, the drug was first sold by Pennsylvania-based William H. Rorer, Inc, which applied the trademark Quaalude to its tablets in 1965. The company incorporated the double-a into the brand name as a way of capitalizing on the success of its antiacid product, Maalox (which is now owned by Novartis Consumer Health). The recommended therapeutic dosage for Quaalude was 150 or 300 mg.
Reports of physiologic addiction to and overdose of methaqualone were published repeatedly in the medical literature, beginning in the late 1960s (for example, here and here). Among Americans, abuse of Quaalude exploded during the 1970s, especially among young adults and teens—who often combined the drug with alcohol for a really soporific buzz. The activity was known as "luding out." The drug also gained a word-of-mouth reputation as an aphrodisiac and enhancer of sexual pleasure (eg, "The Love Drug" or "Heroin for Lovers"); although these effects were overstated, if not outrightly made up. As one young user described her Quaalude experience to the Washington Post in 1978: "I fell asleep."
With the rise of its legitimate and recreational popularity, the unpatented methaqualone was also legally manufactured in the United States by Anar-Stone Laboratories, which called its capsule Sopor (in 75-, 150-, and 300-mg doses). Other American manufacturers of methaqualone compounds included Parke-Davis (Parest) and Wallace (Optimil).
A 1972 Chicago Tribune report ("A Sedative Gains in Drug Culture") indicated that the street cost of methaqualone was 25 or 50 cents per pill. Slang names for the drug included "Rorers" and "seven-fourteens." These terms were derived from the stamp on the branded Quaalude tablet, "Rorer 714." In her grand jury testimony, Polanski's 13-year-old victim reported that the director gave her part of a tablet (dose unknown) that had "Rorer 714" on it.**
According to a 2006 "Frontline" report, high methaqualone demand in the United States was supplied not only by drug firms, but through rogue domestic labs and counterfeit South American operations. In 1981, recreational use of methaqualone was so widespread that it ranked second to marijuana in popularity. The DEA estimated that 80%-90% of the world's methaqualone production was diverted to the illegal drug business. (The DoJ cites the emergence of "stress clinics" in New York, New Jersey, and Florida—essentially B&M equivalents of today's dubious online pharmacies—for the boost of methaqualone abuse in the early 1980s.)
"Frontline" credits the DEA's Gene Haislip with shutting down the illicit methaqualone business in the United States. Haislip successfully convinced foreign manufacturers of the methaqualone powder and their resident countries to stop production. And without the powder, South American producers, like those in Colombia, could no longer pound out pills for export. Simultaneously US physicians began prescribing other hypnotics as sleep aids, and law enforcement shut down the stress clinics. Then in 1984, federal legislation banned the domestic production and sale of methaqualone; in other words, the compound was designated a Schedule I drug.
South Africa is the current hotbed of methaqualone abuse. There the drug is consumed in the form of Mandrax (which combines 250 mg of methaqualone with 25 mg of diphenhydramine). The tablet is typically crushed and snorted or smoked with cannibis.
* Polanski also allegedly plied the girl with champagne. For relevant court records, including Polanski's contemporaneous guilty plea to having sex with a minor, start at thesmokinggun.com.
** Rorer 714 t-shirts were a popular counterculture item.
Image of methaqualone pills attributed to Indiana Prevention Resource Center.
While drugmakers create a vaccine against the currently pandemic swine-flu virus (H1N1 S-OIV 2009), neurologists are advised to monitor the safety of such inoculations, should they be implemented. The caution is founded on a higher-than-expected rate of Guillain-Barre syndrome (GBS) in vaccine recipients during the 1976 immunization campaign against swine flu, reports Neurology Today.
More than 30 years ago, soldiers at Fort Dix, New Jersey, experienced an outbreak of swine flu. Fearing a recurrence of the 1918 influenza epidemic, US government officials implemented a widespread vaccine campaign in which more than 40 million Americans were immunized. However, the drive was aborted after 3 months when reports of GBS in vaccinated individuals emerged. Although GBS surveillance data for the time period are sketchy, evidence suggests that vaccine recipients were significantly more likely to develop the condition within several weeks after inoculation.*
At present, leading neurologists do not anticipate a government-led vaccine campaign against H1N1 S-OIV 2009, given the low mortality rate (0.5%) of the current swine-flu pandemic and the historical risk of GBS with inoculation.
* The typical background rate of GBS is about 1.5 per 100,000 individuals.
[Beat.] How old is it?
Human remains in Rajasthan, India (24°43'N 73°59'E) provide the oldest known evidence of infection with leprosy. Anthropologists from North Carolina and India describe tell-tale signs of bone pathology, consistent with the infection, in a 4000-year-old male skeleton uncovered about 40 km northeast of Udaipur. Findings unearthed at the site of the large Copper Age settlement are described in the latest issue of PLoS One.
The investigators describe widespread evidence for leprosy throughout the bones, including changes in the remarkably intact skull. Findings there are consistent with the characteristic rhinomaxillary syndrome (or leonine facies) of lepromatous leprosy (for an example, see Fig. 1 at link). Other possible infectious causes, like syphilis, leishmaniasis, and TB, were ruled out by the investigators, but additional data to support the conclusion of leprosy will be obtained from any recovered Mycobacterium DNA in the skeleton and geographically related bone collections. The oldest archeological evidence of leprosy, previous to this discovery, dated to the 1st millennium BC in Uzbekistan.
The authors claim that their skeletal remains support contemporaneous Sanskrit text in the Atharva Veda,* which described a plant treatment for leprosy.
Born by night art thou, O plant, dark, black, sable. Do thou, that art rich in colour, stain this leprosy, and the grey spots!...The leprosy which has originated in the bones, and that which has originated in the body and upon the skin, the white mark begotten of corruption, I have destroyed with my charm.
*Dating to the end of the 2nd millennium BC, according to Wikipedia.
Photograph of 4000-year-old skull shows various findings of bony erosion, remodeling, resorption, and necrosis, consistent with lepromatous leprosy.
Since 1937, there have been at least 8 episodes of fatal mass poisoning caused by the oral ingestion of diethylene glycol-tainted drug products; although none has occurred in the United States.
In the summer of 1969, 7 children (ages 6-31 months) died in the area of Cape Town, South Africa, after receiving one or both of 2 liquid sedatives (Pronap or Plaxim). The products were made by the same pharmaceutical firm, which had substituted diethylene glycol for propylene glycol (the latter being an FDA-approved solvent for drugs, cosmetics, and food). Attempted treatment included rehydration, correction of metabolic acidosis, peritoneal dialysis (in 2 cases), and life support.
In 1986, 14 inpatients in a Bombay (Mumbai) hospital died of acute renal failure after receiving in-house glycerin therapy. The glycerin—which contained 18.5% diethylene glycol, 51% polyethylene glycol, and 9% glycerin—was purchased by the hospital through intermediary brokers, who had bought the product on the cheap from an industrial producer in India. Treatment with sodium bicarbonate, various diuretics, and dialysis (in 12 cases) was unsuccessful.
Between June and September of 1990, 47 children died at a Nigerian teaching hospital after ingesting paracetamol syrup that was tainted with diethylene glycol. Treatment consisted of rehydration and correction of acidosis, but none underwent dialysis. All died within 2 weeks of admission. (In a related incident, 109 Nigerian children died the same year after consuming ethylene glycol-tainted cough syrup.)
Beginning in 1990, a significant rise in the incidence of unexplained renal failure in Bengalese children was believed to be due to the ingestion of various brands of paracetamol elixir that were tainted with diethylene glycol. At least 67, and as many as 272, children were affected. After the government banned the sale of paracetamol elixirs in December 1992, pediatric hospitalizations for unexplained renal failure dropped by 84%.
In 1992, 29 people in Argentina died of acute renal failure as a result of consuming diethylene glycol-tainted propolis syrup. A study of 15 adult victims revealed a "good correlation" between the amount of diethylene glycol ingested and the anion gap. Syrup samples contained 65% diethylene glycol (w/v), and victims took between 5 and 20 mL. Therefore, the lethal dose of diethylene glycol for adults was estimated at 0.014-0.170 mg/kg body weight.
An increase in the incidence of unexplained renal failure in Haiti led to the discovery of diethylene glycol-induced disease in 109 children (ages 1 month-13 years) from the fall of 1995 to July 1996. The ingestion of locally made acetaminophen syrups (Afebril and Valodon) was significantly associated with the condition. Analysis revealed that these formulations were made with diethylene glycol-contaminated glycerin, which had been imported from a Chinese manufacturer by way of Europe. The median concentration of diethylene glycol in the final products was 14.4% (range, 1.2%-19.6%). The median estimated dose of consumed diethylene glycol (n = 32) was 1.34 mL/kg (range, 0.22-4.42 mL/kg), but toxic doses were often less than 1 mL/kg. The death rate among the children who remained in Haiti was 98% (85 of 87*). Among the 11 children transported to the United States for treatment, 8 survived, and 7 recovered renal function.
In 1998, 36 Indian children developed acute renal failure after consuming a diethylene glycol-tainted cough syrup, which was produced by a company in Gurgaon; 33 of these children died despite undergoing peritoneal dialysis. How and when diethylene glycol entered the syrup was unknown at the time of the medical report.
In the fall of 2006, an investigation into cases of unexplained renal failure in Panama ultimately led to the discovery of more than 100 deaths due to the consumption of cough syrup made with Chinese-imported glycerin. The glycerin, which was sold to the Panamanian health service, was incorporated into 260,000 bottles of the medicine. In its investigation, the New York Times traced 46 barrels of imported glycerin stock, labeled as 99.5% pure but containing ~24% diethylene glycol, from a Panamanian port to the Taxing Glycerine Factory in the Yangtze Delta (by way of Barcelona). A Panamanian government report released last year concluded that at least 174 people were poisoned and 115 were killed (66% death rate) as a direct result of the contaminated syrup (Bogdanich W. Panama releases '06 report on poisoning. NYT, February 14, 2008).
*****************************************************************************
The toxicity of diethylene glycol is believed to be due to its metabolite, HEAA—which is produced by the enzymatic activity of ADH and ALDH. But how HEAA produces cellular dysfunction is unclear, according to Kraut et al. Like other alcohols, diethylene glycol is rapidly absorbed from the gut and has a low volume of distribution (0.5 L/kg). Animal studies indicate that 30%-50% of diethylene glycol is eliminated through the liver, and 50%-70% via the kidneys. Although toxic and lethal doses in humans have been estimated in some reports of mass poisoning, susceptibility to diethylene glycol appears to vary widely for reasons that remain unknown.
Animal studies also indicate that the administration of ADH and ALDH inhibitors (eg, fomepizole) may prevent the production of HEAA, and dialysis (with or without fomepizole) has been used successfully in patients with diethylene glycol poisoning. Dialysis is not only instituted for renal failure, but may remove diethylene glycol and its toxic metabolite.
ADH = alcohol dehydrogenase; ADLH = aldehyde dehydrogenase; HEAA = 2-hydroxyethoxyacetic acid.
* Follow-up was unavailable for 11 children.
Depicted chemical structure of diethylene glycol from Wikipedia.
January 10, 1939: Three months after Dr. Samuel E. Massengill pleaded guilty to 174 counts of adulterating and misbranding Elixir Sulfanilamide, he was elected president of the Bristol Chamber of Commerce in a show of municipal confidence [1].
January 17, 1939: Former Massengill chemist and creator of Elixir Sulfanilamide, Harold Cole Watkins, 58, shot himself in the heart with a .38 caliber automatic pistol at 7:30 am in the kitchen of his Bristol home. Watkins had "retired" from the Massengill company 6 months earlier; the circumstances of his departure from the firm, whether voluntary or by request, were not clear. Although the death was reported a suicide, Watkins's wife claimed that the self-inflicted gunshot was accidental. In addition to his widow, Watkins was survived by 2 sons [2-4].
January 19, 1939: Massengill sales manager Gordon Fletcher reported that the company had paid out more than $500,000 in injury claims regarding Elixir Sulfanilamide [4].
April 14, 1939: In the District Court for the Northeastern Division of the Eastern District of Tennessee (at Greeneville), judge George C. Taylor* ordered Massengill to pay $8500** and court costs for the wrongful death of Earl L. Beard, who had died in a Tulsa hospital on October 16, 1937, after consuming Elixir Sulfanilamide. The suit was brought by the deceased's mother, Mrs. Norris T. Beard of Oklahoma City [5]. (The plaintiff, represented by Swingle and Hardin of Greeneville, originally filed the suit in September 1938 and asked for $50,000.)
April 19, 1939: A civil suit brought by the widow and heirs of John W. Gibbons of Mt. Olive, Mississippi, against Massengill was dismissed without prejudice in the same federal court. Gibbons, 71, had died October 9, 1937, after consuming 2.5 ounces of a 4-ounce elixir prescription, which had been written by his physician, Archie Calhoun. (The civil complaint, originally filed on October 1, 1938, asked for a total of $45,000 in damages and a jury trial.) The plaintiffs moved for a voluntary nonsuit, most likely on the basis of deposition testimony. One of the deceased's physicians testified that Gibbons had died of coronary thrombosis, which was believed to be independent of diethylene glycol toxicity. A treating urologist also suspected prostate cancer. The plaintiffs were required to pay court costs [5].
April 20, 1939: A civil complaint was filed against Massengill in the same federal court by Claire B. Williams, widow of Fred L. Williams, a Florida resident who had died October 12, 1937, after consuming probably 6 ounces of Elixir Sulfanilamide. The plaintiff, represented by Caldwell, Brown, and O'Dell of Bristol, Tennessee, demanded $10,000 and court costs. Three months later, the case was settled out of court for an undisclosed amount [5].
November 3, 1939: A civil complaint was filed against Massengill in the same federal court by Sylvia Cauley, who alleged the wrongful death of her husband, Emanuel Cauley. Cauley, a Florida resident, had died October 16, 1937, after consuming 5 ounces of Elixir Sulfanilamide. The plaintiff, also represented by Caldwell, Brown, and O'Dell, demanded $10,000 and court costs. Massengill defended the suit by arguing that the 1-year Tennessee statute of limitations applied, not the 2-year limit in Florida. Judge Taylor agreed, and the suit was dismissed in March of 1940. The plaintiff was ordered to pay court costs [6].
Also in November, Theodore Klumpp, Chief Medical Officer of the FDA, and Herbert Calvery published their report on the Elixir Sulfanilamide deaths, which included information from 353 persons who consumed the drug. Data were "sufficient" to conclude that Elixir Sulfanilamide was the primary cause of 105 deaths; although in "several" cases, concomitant illness may have contributed to mortality. The drug was most often prescribed for the treatment of gonorrhea (39% of deaths) or sore throat (23% of deaths). The average time of survival from the first elixir dose to death was 9.4 days (range, 2-22 days) [7].
The most common, initial symptoms were nausea and vomiting—symptoms which may have been life saving for some by prompting discontinuation of the drug. Headache was also frequently experienced. These symptoms were followed by a progressive decrease in urine output, which was often associated with considerable back, flank, and/or abdominal pain. Signs of uremic encephalopathy then emerged, leading to coma, convulsions, and death. In only a few cases were laboratory studies performed (eg, South Carolina case report).
The average elixir dose taken by the deceased, both children and adults, was somewhat higher than that taken by the 248 survivors, although there was considerably overlap in the range of doses taken by the 2 groups.
|
Group |
Mean Dose, cc |
Minimum Dose, cc |
Maximum Dose, cc |
|
Deceased |
|
|
|
|
7 months-16 years |
52.7 ± 32.8 |
5 |
120 |
|
17-78 years |
98.6 ± 37.9 |
20 |
240 |
|
Survivors |
|
|
|
|
1-14 years |
44.2 ± 30.2 |
3 |
105 |
|
≥15 years |
83.7 ± 57.5 |
1 |
240 |
March 8, 1940: A civil complaint was filed against Massengill in the District Court for the Northeastern Division of the Eastern District of Tennessee (at Greeneville) by the administrator for Pearl Locklair. Locklair died October 4, 1937, in Charleston, SC, after consuming an unknown quantity of Elixir Sulfanilamide. The plaintiffs asked for $35,000 in total damages. Massengill defended the complaint by arguing that the 1-year Tennessee statute of limitations applied, not the 6-year limit in South Carolina. Judge Taylor agreed, and the suit was dismissed on August 7, 1940. The plaintiff appealed to the US Court of Appeals for the Sixth Circuit [5,8].
January 9, 1942: The US Court of Appeals for the Sixth Circuit reversed the lower court's decision, and the wrongful death suit for Pearl Locklair was remanded for trial [8].
May 25, 1942: Massengill's petition to the US Supreme Court in the wrongful death suit for Pearl Locklair was denied [9].
September 2, 1942: In a settlement with the administrator for Pearl Locklair, Massengill agreed to pay $1500, plus $150 in expenses and court costs [5].
* The same judge who presided over the government's adulteration and misbranding case against Massengill. The Beard judgment was the result of a non-jury decision.
** $7500 for loss of support and other pecuniary loss and $1000 for pain and suffering.
1. Massengill heads Bristol chamber. Bristol Herald Courier. January 11, 1939; p 5, cols 1-3.
2. H. C. Watkins victim wound. Bristol News Bulletin. January 17, 1939; p 1, col 6.
3. Harold Cole Watkins victim of gunshot. Bristol Herald Courier. January 18, 1939; p 2, col 2.
4. Maker sulfanilamide formula is suicide. Greeneville Sun. January 19, 1939; p 1, col 6.
5. Greeneville, TN, court records; obtained from NARA.
6. Cauley v S. E. Massengill Co. 35 F 371 (TN Dist 1940).
7. Klumpp TG, Calvary HO. The toxicity for human beings of diethylene glycol with sulfanilamide. South Med J. 1939;32:1105-1109.
8. Wilson v Massengill. 124 F2nd 666 (US App 1942).
9. Massengill v Wilson. 316 US 686; 62 S Ct 1274; 86 L Ed (US SC 1942).
In a way that only grand tragedy can instigate reform, the rising number of deaths due to Massengill's Elixir Sulfanilamide mobilized a formerly apathic press and public to demand revision of the 30-year-old Wiley statute. The principal House opponent of Copeland's first S. 5 bill, B. Carroll Reece (R-TN), was particularly stung by the fact that Massengill's company resided in his district, and reformists were only too happy to point out this fact.
But passage of S. 5, while facilitating the FDA's ability to seize bottles of Elixir Sulfanilamide, would not have prevented the disaster. The bill, unlike the original Tugwell measure (S. 1944), had no licensing provisions for new drugs entering the market, as the League of Women Voters was quick to note. This fact was verified by Representative Lea with Paul Dunbar of the FDA, and the California legislator requested an appropriate amendment to rectify the omission.
Copeland was way ahead; on December 1, he introduced S. 3073, which stated that any manufacturer who sought to market a new drug must submit the drug's components, testing records, an explanation of the manufacturing processes, labeling examples, and drug samples (if requested) to the Secretary of Agriculture. Five months later, the Senate passed S. 3073 unanimously, after a few minutes of half-hearted objections.
However, the old sticking point of the government's advertising purview remained, manifest in the Wheeler-Lea bill (S. 1077)—which was intended to expand the FTC's control over food, drug, and cosmetic advertising. After heated debate, the House had passed the measure in January of 1938, and the Senate had followed 2 months later. The bill was signed into law on March 21. The FDA was "apoplectic," given that the act not only stripped the agency of any marketing control over drugs but required proof of fraudulent intent after the fact (like the 1912 Sherley amendment).*
By the spring of 1938, Lea, after increasing pressure, finally brought S. 5 no. 2 out of House committee, but not before he had slipped in a section that allowed for numerous appeal reviews for alleged violators in any one of the 85 federal district courts. Lea's rationale was to provide a check on the Secretary of Agriculture's regulatory power, but reformists were having none of it. Consumer and national women's organizations were outraged and bombarded the President with pleas to intervene. FDR did so, although somewhat cryptically. Publicly he gave no indication that he would sign the Copeland-Chapman bill if Lea's appeal section was included; privately he informed the House committee of a forthcoming veto.
So in June, a legislative compromise was hammered out in conference: industry's appeals would be restricted by circumstance and court venue. And in a conciliatory mood, the conferees also accepted stronger language on the subjects of label disclosure, standard variations, and seizures. The conference report was quickly passed by the Senate and House, and FDR signed the new Food, Drug and Cosmetic Act on June 25, 1938—12 days after Massengill pleaded not guilty to federal charges of mislabeling and misbranding Elixir Sulfanilamide and 8 days after an exhausted Royal Copeland collapsed on the Senate floor and died later that evening. He was 69.
The Act that Copeland championed would become effective 1 year later.
* Regulation of prescription-drug advertising was finally transferred to the FDA after passage of the Kefauver-Harris Drug Amendments in 1962.
Chief source: Jackson Co. Food and Drug Legislation in the New Deal. Princeton, NJ: Princeton University Press; 1970.
With the input of the FDA and the influence of the all-important women's groups (who had the backing of Eleanor Roosevelt), S. 5 no. 2 was strengthened in committee on the points of misbranding and seizures. The bill was passed by the upper chamber on March 9, 1937, and forwarded to the House, where the FTC had historically exerted its influence to retain advertising control.
The power struggle between the FDA and the FTC was further complicated by the simultaneous introduction of the Wheeler-Lea bill, which was drafted to expand the FTC's authority. The measure (S. 1077), spearheaded by Senator Burton Wheeler (D-MT) and Representative Clarence Lea (D-CA), was sent to the House after Senate passage on March 29, 1937. The timing meant that both the Copeland-Chapman bill and the Wheeler-Lea bill would be debated in House committee at the same time—in this case, mid-May of 1937. Political maneuvering between the Chapman and Lea camps would keep both measures in House limbo when Massengill's Elixir Sulfanilamide hit the market during the fall of 1937.
* From January 1935 to October 1936, 92 drug-related laws had passed in 39 states.
Chief source: Jackson Co. Food and Drug Legislation in the New Deal. Princeton, NJ: Princeton University Press; 1970.
In the summer of 1935, the House conducted hearings on Copeland's latest food and drug bill, S. 5. Chairing the hearings was Representative Virgil Chapman (D-KY), a lawyer and newcomer to food and drug reform. Chapman, however, was quick on the uptake. He rapidly grasped the thorny issues that impeded the passage of effective reform—particularly the conflict between the FTC and the FDA for advertising control. S. 5's best chance for passage, he concluded at the end of the hearings, lay in a quiet education campaign, until sufficient House support was confirmed.
In the meantime, Chapman held the bill in committee, where efforts were made to strengthen the drug variation and seizure clauses. But the chief question remained: Who would control drug advertising, the FTC or the FDA? The President offered little in the way of decisive input, and after 9 months, Campbell's agency ultimately lost its fight for purview over advertising.
On May 22, 1936, the House version of S. 5 was finally reported out of committee, with a minority dissent (led by Virgil Chapman) on the advertising section. In mid-June, this version of the bill was passed in the House, after which time Senate and House conferees met to hammer out a compromise on the amendments—and specifically, on the issue of advertising oversight. After considerable wrangling, the final bill stipulated that all health-related advertising would be regulated by the FDA; the FTC would oversee the marketing of food and cosmetics.
Although the Senate accepted the compromise, fierce opposition to the advertising agreement was led in the House by lawyers B. Carroll Reece (R-TN) and Samuel D. McReynolds (D-TN). Both men represented districts in East Tennessee, the home of influential FTC member Ewin L. Davis. Reece's district was also the headquarters of the S. E. Massengill Company, in Bristol.* Their arguments, which drew on FTC loyalty and fears of Tugwell, were persuasive; in the summer of 1936, the House killed S. 5 in an overwhelming vote.
* In November 1937, Massengill would deny any attempted influence on Reece regarding passage of a food and drug law: "I have never, directly or indirectly, opposed any proposed Food and Drug law. I never spoke to Hon. Carroll Reece, my congressman, about the one now pending, nor, to my knowledge, did any of my friends do so."
Chief source: Jackson Co. Food and Drug Legislation in the New Deal. Princeton, NJ: Princeton University Press; 1970.
Photograph of Virgil Chapman from the Biographical Directory of the US Congress.
