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Steven THOMAS, a Minor, by his Guardian ad Litem, Susan M. Gramling, Plaintiff-Appellant-Petitioner,
v.
Clinton L. MALLETT, Billie R. Mallett, and Germantown Mutual Insurance Co., Defendants,
AMERICAN CYANAMID Co., Atlantic Richfield Co., E.I. DuPont De Nemours and Co., NL Industries, Inc., SCM Chemicals, Inc., Sherwin-Williams Co., ConAgra Grocery Products Co., Defendants-Respondents.
Supreme Court of Wisconsin.
For the plaintiff-appellant-petitioner there were briefs by Peter G. Earle and Law Offices of Peter Earle, Milwaukee; and Robert J. McConnell, Fidelma Fitzpatrick and Motley Rice, LLC, Providence, RI, and oral argument by Peter G. Earle and Robert J. McConnell.
For the defendants-respondents, Atlantic Richfield Company, E.I. du Pont de Nemours & Co., Con-Agra Grocery Products Company, NL Industries, Inc., American Cyanamid Co., and Millennium Inorganic Chemicals, Inc. (f/k/a SCM Chemicals, Inc.) there was a brief by Philip H. Curtis, Bruce R. Kelly and Arnold & Porter, New York, NY, David G. Peterson, Michael B. Apfeld *243 and Godfrey & Kahn, Milwaukee (on behalf of Atlantic Richfield Company); William H. King, Jr., Steven R. Williams, Joy C. Fuhr and McGuire Woods LLP, Richmond, VA, M. Christine Cowles and Quarles & Brady LLP, Milwaukee (on behalf of E.I. du Pont de Nemours Co.); James P. Fitzgerald, John J. Schirger and McGrath, North, Mullin & Kratz, Omaha, NE, Paul Benson and Michael Best & Friedrich, Milwaukee (on behalf of Con-Agra Grocery Products Company); Susan McGuire and Kirland & Ellis, Washington, D.C., Donald E. Scott, Jennifer Heisinger, Elizabeth L. Thompson and Bartlit Beck Herman Palenchar & Scott, Denver, CO, David G. Peterson, Michael B. Apfeld and Godfrey & Kahn, Milwaukee (on behalf of NL Industries, Inc.); Richard W. Mark, Elyse Echtman and Orrick Herrington & Sutcliffe LLP, New York, NY, David G. Peterson, Michael B. Apfeld and Godfrey & Kahn, Milwaukee (on behalf of American Cyanamid Co.); and Michael T. Nilan, Cortney G. Sylvester and Halleland Lewis Nilan Sipkins & Johnson, Minneapolis, MN, James R. Clark, Trevor J. Will and Foley & Lardner, Milwaukee (on behalf of Millennium Inorganic Chemicals Inc. (f/k/a SCM Chemicals, Inc.) and oral argument by Bruce Kelly (on behalf of American Cyanamid Co., et al.).
For the Sherwin-Williams Company there was a brief by Frank J. Daily, David B. Bartel, Jeffrey K. Spoerk, Daniel I. Hanrahan, and Quarles & Brady LLP, Milwaukee; and Paul Michael Pohl, Charles H. Moellenberg, Jennifer B. Flannery and Jones Day, Pittsburgh, PA, and oral argument by Charles H. Moellenberg, Jr.
An amicus curiae brief was filed by Anne Berleman Kearney, Joseph D. Kearney and Appellate Consulting Group, Milwaukee, on behalf of Civil Trial Counsel of Wisconsin.
*244 An amicus curiae brief was filed by James A. Buchen, Madison, on behalf of Wisconsin Manufacturers & Commerce.
An amicus curiae brief was filed by Gerardo H. Gonzalez, Richard H. Porter, Chris J. Trebatoski and Gonzalez, Saggio & Harlan, L.L.P., Milwaukee, on behalf of the African-American Chamber of Commerce, Inc. and the Hispanic Chamber of Commerce of Wisconsin, Inc.
An amicus curiae brief was filed by Lynn M. Novotnak and First, Blondis, Albrecht & Novotnak, S.C., Milwaukee, on behalf of Service Employees International Union-Wisconsin State Council, Wisconsin Commission on Occupational Safety and Health, Repairers of the Breach, Wisconsin Citizen Action, American Federation of Teachers, Local 212, and Sixteenth Street Community Health Center.
An amicus curiae brief was filed by Mark S. Olson and Oppenheimer Wolff & Donnelly LLP, Minneapolis, MN; James M. Beck and Dechert LLP, Philadelphia, PA; Hugh F. Young, Jr., Reston, VA, on behalf of Product Liability Advisory Council, Inc.
*242 ¶ 1. LOUIS B. BUTLER, JR., J.
Steven Thomas, by his guardian ad litem, seeks review of a published court of appeals decision[1] that declined to extend the risk-contribution theory announced in Collins v. Eli Lilly Co., 116 Wis. 2d 166, 342 N.W.2d 37 (1984), to the defendant-respondent lead pigment manufacturers, American Cyanamid Co., Atlantic Richfield Co., ConAgra Grocery Products Co., E.I. DuPont De Nemours and Comp., NL Industries, Inc., SCM Chemicals, Inc., and Sherwin-Williams Co. (collectively "Pigment Manufacturers"). *245 The court of appeals concluded that because Thomas had a remedy against his landlords for their negligence in failing to abate lead paint hazards in his prior residences, there was no reason to extend Collins' risk-contribution theory. The court of appeals also concluded that Thomas could not proceed on his claims of civil conspiracy and enterprise liability.
¶ 2. Thomas argues this court should reverse the court of appeals' decision because (1) although he received a remedy from his landlords for their negligence, Article I, Section 9 of the Wisconsin Constitution does not foreclose his seeking a remedy for the Pigment Manufacturers separate wrong for producing and promoting toxic lead pigments; (2) Collins' risk-contribution theory should be recognized for white lead carbonate claims; and (3) he has presented sufficient material facts to warrant a trial on his alternative theories of liability of civil conspiracy and enterprise liability.
¶ 3. We agree with Thomas that Article I, Section 9 does not insulate wrongdoers from liability simply because recovery has been obtained from an altogether different wrongdoer for an altogether different wrong. We also conclude that the white lead carbonate claims at issue in this case are factually similar enough to Collins to warrant extension of the risk-contribution theory. However, we do not agree that Thomas has presented sufficient material facts to warrant a trial on his civil conspiracy and enterprise liability claims. Therefore, we affirm in part and reverse in part the court of appeals' decision.[2]
*246 I
¶ 4. Because this case is before us on summary judgment, we construe all facts and reasonable inferences in the light most favorable to the nonmoving party, which in this case is Thomas.[3]See Strozinsky v. Sch. Dist. of Brown Deer, 2000 WI 97, ¶ 32, 237 Wis. 2d 19, 614 N.W.2d 443.
¶ 5. Thomas was born on June 23, 1990. He claims that he sustained lead poisoning by ingesting lead paint from accessible painted surfaces, paint chips, and paint flakes and dust at two different houses he lived in during the early 1990's.
¶ 6. In August 1991, while living at 2652 North 37th Street, Milwaukee, Wisconsin, 14-month-old Thomas exhibited an early onset of childhood lead poisoning, with his blood lead levels (BPb) at 18 µg/dl. Thomas's cognitive skills were tested, which identified cognitive deficits in perceptual organization, visual motor integration, expressive language, academic and fine motor skills coupled with an attention deficit hyperactivity disorder. Eight months later, at the end of April 1992, his BPb increased to 40 µg/dl.
¶ 7. Thomas continued to live at 2652 North 37th Street until January 1993. This house was built in 1905. City of Milwaukee Health Department documented lead-based violations at this home on July 29, 1992.
*247 ¶ 8. Thomas's next known phase of lead poisoning occurred while he was living at 2654 North 25th Street, Milwaukee, Wisconsin. That house was built in 1900. Lead-based paint violations were documented at this residence on August 12, 1993.
¶ 9. While Thomas's BPb decreased by January 1993 to 27 µg/dl, it rose to 49 µg/dl by July 1993. Thomas was admitted to Children's Hospital of Wisconsin for five days of chelation treatment.
¶ 10. From mid-August 1993 to early September 1993, Thomas's BPb rose from 13 µg/dl to 33-40 µg/dl. From August 1993 until November 1993, Thomas lived at 4736 North 37th Street, Milwaukee, Wisconsin. Thereafter, Thomas's BPb steadily declined but was still in the BPb range for lead poisoning.
¶ 11. According to Dr. John F. Rosen, a professor of pediatrics and head of the Division of Environmental Sciences at the Children's Hospital at Montefiore of the Albert Einstein College of Medicine, Thomas's cognitive deficits are a "signature or constellation of cognitive effects" that are typical of lead poisoning. In Thomas's case, Rosen states that these deficits are permanent. In addition, due to Thomas's elevated BPb over the extended period of time, Thomas will require lifetime medical monitoring-surveillance for physical disorders, as he is now at a high risk for developing future medical complications, including kidney disease, peripheral neuropathy, hypertension, and cardiovascular disease. Rosen opines that Thomas's high lead levels are exclusively derived from ingesting lead based pigments in paint.[4]
*248 ¶ 12. Thomas subjected various paint samples from his prior residences to chemical analysis. Robert Dragen, an electron microscopist, analyzed the various paint layers contained in the samples and provided the elemental composition for each layer. According to that *249 analysis, none of the paint layers contained detectable levels of sulfur or chromium. Thus, according to Dr. Paul Mushak, a toxicologist and human health risk assessment specialist, this analysis conclusively rules out lead sulfate or lead chromate pigments. These pigments along with white lead carbonate pigments were the essential lead pigments used for residences. White lead carbonate was the principal pigment used, however. Because lead sulfate and lead chromate could be empirically excluded, Mushak opines to a reasonable degree of scientific and technological certainty that the houses contain lead paint made with white lead carbonate pigment.[5]
*250 ¶ 13. As noted, the houses where Thomas alleges he ingested lead paint were built in 1900 and 1905. During that period, use of lead paint for residences was common. Lead paint contained up to 50 percent lead pigment and maintained widespread use through the 1940s. The use and manufacturing of interior lead-based paints declined during the 1950s, and, in 1955, the lead industry voluntarily adopted a standard of the American National Standards Institute that limited lead content to a maximum of one percent in paints intended for children's toys, furniture, and interior surfaces. However, lead paint for interiors continued to be available until the 1970s.
¶ 14. As of December 31, 1972, lead paint for interior and exterior household use containing more than 0.5 percent lead of its total weight was banned from interstate commerce. 16 C.F.R. § 1500.17(a)(6)(i)(B) (2005). In 1978, the ban was expanded to residential use of paint containing more than 0.06 percent lead by weight. 16 C.F.R. § 1303.2(2) (2005); 16 C.F.R. § 1303.4 (2005). In 1980, Wisconsin banned the use of lead paint. Wis. Stat. § 254.12 (2003-04);[6]Antwaun A. v. Heritage Mut. Ins. Co., 228 Wis. 2d 44, 61, 596 N.W.2d 456 (1999).
¶ 15. On December 4, 1996, prior to commencing the action that is the subject of this appeal, Thomas settled with Fire Insurance Exchange, the insurer for the landlord of 2652 North 37th Street, on a Pierringer[7] basis for $62,652.55. On September 10, 1999, Thomas commenced the underlying action against his remaining two landlords and their insurers and the Pigment Manufacturers for the injuries he received from lead *251 poisoning. As to his landlords, Thomas alleged that they negligently maintained the premises with respect to lead paint. As to the Pigment Manufacturers, Thomas alleged that they were liable for his injuries on the basis of, among other claims, strict liability, negligence, civil conspiracy, and enterprise liability.
¶ 16. On June 26, 2000, the Milwaukee County Circuit Court, Honorable Patricia D. McMahon, dismissed State Farm Insurance Co., the insurer for the landlord at 4736 North 37th Street, based on a pollution exclusion in its policy.[8] Thomas subsequently abandoned his claims against that landlord. On August 8, 2002, Thomas settled his claim with Germantown Mutual Insurance, the insurer for the landlord of 2654 North 25th Street, on a Pierringer basis for $261,520. Thus, the only remaining defendants were the Pigment Manufacturers.
¶ 17. Although all of the Pigment Manufacturers or their predecessors-in-interests[9] manufactured white lead carbonate at various times during the existence of *252 Thomas's prior residences, Thomas conceded that he cannot identify the specific pigment manufacturer that produced the white lead carbonate he ingested. The Pigment Manufacturers moved for summary judgment, arguing, as relevant here, that Thomas could not prove causation in fact or proximate cause; Collins should not be extended as Thomas already obtained a remedy from his landlords; Collins should not be extended outside the unique circumstances of diethylstilbestrol (DES); and that Thomas's civil conspiracy and enterprise liability claims were deficient. The Milwaukee County Circuit Court, Honorable Timothy G. Dugan, granted the motion.
¶ 18. The circuit court concluded that the DES fact situation in Collins was too different from the circumstances of Thomas's lead paint claims. First, the circuit court concluded that unlike the situation in Collins, where the plaintiff was remediless without the risk-contribution theory, Thomas had a remedy against the negligent landlords. Second, the circuit court noted that Collins concerned a nine-month window during which an expectant mother consumed DES, whereas here, since the houses Thomas lived in were constructed in 1900 and 1905, the lead paint could have been applied anytime during what was approaching a one hundred year time span. The court concluded the Pigment Manufacturers had no real defense, unlike in Collins. Third, the circuit court determined that DES produced a rare form of cancer, whereas lead poisoning could be caused by any number of lead products and *253 thus did not produce a "signature injury." Fourth, the circuit court concluded that all DES was identical, whereas there were different forms of lead pigments that were used in varying amounts by paint manufacturers. Fifth, unlike DES manufacturers, the circuit court noted that the Pigment Manufacturers were not in exclusive control of the risks involved as they did not make the finished paint product or ensure that the product was properly maintained in homes.
¶ 19. The circuit court then concluded that Thomas's civil conspiracy claim failed because he could not prove an underlying tort. Further, the circuit court determined that Thomas did not present clear evidence of an agreement between the Pigment Manufacturers to accomplish an unlawful purpose. Finally, the circuit court also determined that the enterprise liability was not available, as there was no industry standard for white lead carbonate pigment.
¶ 20. Thomas appealed, and the court of appeals affirmed. Thomas v. Mallett, 2004 WI App 131, ¶ 7, 275 Wis. 2d 377, 685 N.W.2d 791.
¶ 21. The court of appeals agreed with Thomas that his case had many characteristics in common with Collins, writing:
As Thomas points out in his extensive submissions, and, for the purposes of this appeal, assuming their verity, this case and Collins share, for many of the same reasons, the inability of the plaintiff to identify those who made and sold the specific substance alleged to have caused injury. Thus, in both Collins and here the substances produced or sold by one company are, as material to the possibility of tracing the manufacturer or seller, essentially the same as that produced or sold by the others. . . . Additionally, both the diethylstilbestrol alleged to have caused the plaintiff's vaginal *254 cancer in Collins, and the white lead carbonate alleged to have caused Thomas's neurological disorders were made and sold by many companies long before the injury, making it impossible to trace specific manufacturers or sellers to the particular injury-causing product.
Id., ¶ 4.
¶ 22. These similarities aside, however, the court of appeals read Collins as fashioning the risk-contribution theory for situations where a plaintiff is without any remedy whatsoever. Id., ¶ 5. Because Thomas already had an existing right against his landlords, the court of appeals determined that recognizing Collins' risk-contribution theory for white lead carbonate was unnecessary. Id., ¶ 7.
¶ 23. Regarding Thomas's civil conspiracy claim, the court of appeals agreed that he presented sufficient evidence to create a genuine issue of material fact as to whether the Pigment Manufacturers acted in concert to at least minimize the dangers of white lead carbonate. Id., ¶ 9. However, the court of appeals determined that Thomas did not establish that the concerted action was a substantial factor in producing his injuries. Id., ¶¶ 9-13. Specifically, the court of appeals concluded that Thomas had not shown that the conspiracy was a substantial factor that contributed to either the use of lead-based paint or its faulty maintenance. Id., ¶ 13.
¶ 24. Finally, the court of appeals rejected Thomas's enterprise liability theory for two reasons: first, Thomas did not produce any evidence that white lead carbonate either was negligently made or dangerously defective if the lead paint was properly applied and maintained, id., ¶ 17; and second, there was no need to *255 allow Thomas to sue on an enterprise liability theory as he already had a remedy at law for his injuries against the landlords, id., ¶ 18.
¶ 25. Thomas seeks review.
II
¶ 26. As noted, this case is before us on summary judgment. We review summary judgments independently, applying the same methodology as the circuit courts. Mayberry v. Volkswagen of Am., Inc., 2005 WI 13, ¶ 15, 278 Wis. 2d 39, 692 N.W.2d 226; Green Spring Farms v. Kersten, 136 Wis. 2d 304, 315, 401 N.W.2d 816 (1987). Summary judgment must be entered "if the pleadings, depositions, answers to interrogatories, and admissions on file, together with the affidavits, if any, show that there is no genuine issue as to any material fact and that the moving party is entitled to a judgment as a matter of law." Wis. Stat. § 802.08(2). All reasonable inferences drawn from the underlying facts must be viewed in the light most favorable to the non-moving party. Grams v. Boss, 97 Wis. 2d 332, 338-39, 294 N.W.2d 473 (1980).
III
¶ 27. A problem facing Thomas, who alleges that he was injured by white lead carbonate pigment, is that he is unable to identify the precise producer of the white lead carbonate pigment he ingested at his prior residences due to the generic nature of the pigment, the number of producers, the lack of pertinent records, and the passage of time. See Collins, 116 Wis. 2d at 177. Some courts have simply denied extension of market-share liability under these circumstances and thus denied *256 lead pigment plaintiffs recovery.[10] However, the question presented is whether Collins' risk-contribution theory should be extended to white lead carbonate claims. We agree that it should.
¶ 28. The following backdrop provides the relevant context for determining whether Collins' risk-contribution theory should be recognized for white lead carbonate claims.[11] It is by no means a complete discussion of the history of white lead carbonate, but rather is assembled pursuant to our standard of review that the facts are to be construed in the light most favorable to Thomas as the nonmoving party.[12]See Grams, 97 Wis. 2d at 339.
*257 A. The Problem of Lead Poisoning from Lead-Based Paints.
¶ 29. According to the Center for Disease Control's ("CDC"s") Preventing Lead Poisoning in Young Children, 1 (Oct. 1991) (hereinafter "Preventing Lead Poisoning"), it is well-recognized that given children's rapidly developing nervous systems, "[c]hildren are particularly susceptible to lead's toxic effects." Id. Because the human body cannot differentiate between lead and calcium, after lead has remained in the bloodstream for a few weeks, it is then absorbed into bones, where it can collect for a lifetime. EPA, Lead In Your Home: A Parent's Reference Guide, 4 (June 1998). Once lead enters the child's system, more lead is absorbed than would be in adults. Preventing Lead Poisoning, 11.
¶ 30. Children "are more exposed to lead than older groups because their normal hand-to-mouth activities may introduce many nonfood items into their gastrointestinal tract." Id. The CDC noted that "[p]ica, the repeated ingestion of nonfood substances, has been implicated in cases of lead poisoning; however, a child does not have to eat paint chips to become poisoned." Id., 18. It is more common for children to ingest dust and soil contaminated with lead from paint that either has flaked or chalked as it aged or has been otherwise disturbed during home maintenance or renovation. Id., 18. "This lead-contaminated house dust, ingested via normal repetitive hand-to-mouth activity, is now recognized as a major contributor to the total body burden of lead in children." Id., 18. Thus, "[b]ecause of the critical role of dust as an exposure pathway, children living in *258 sub-standard housing and in homes undergoing renovation are at particular risk for lead poisoning." Id., 18.
¶ 31. The consequences of child lead poisoning are well documented. According to the CDC:
Very severe lead exposure in children (blood lead levels ≥80µg/dL) can cause coma, convulsions, and even death. Lower levels cause adverse effects on the central nervous system, kidney, and hematopoietic system. Blood lead levels as low as 10µg/dL, which do not cause distinctive symptoms, are associated with decreased intelligence and impaired neurobehavioral developments.
Id., 9. The CDC also states that "the weight of the evidence clearly supports the hypothesis that decrements in children's cognition are evident at blood lead levels well below 25 g/dL." Id.
¶ 32. Although lead can originate from many different materials, such as food, soil, water, or air, lead paint is the primary culprit. The CDC concluded that "[l]ead-based paint is the most common source of high-dose lead poisoning." Id., 65. "Numerous studies have established that the risk of lead poisoning is related to the presence of lead-based paint and to the condition of such paint." Id., 18. As the United States Department of Health and Human Services determined in Toxicological Profile for Lead, 407 (July 1999):
[T]he most common source of lead exposure for children is lead-based paint that has deteriorated into paint chips and lead dusts and that the most common sources of lead exposure for adults are occupational.
Similarly, in 1990, the Food and Drug Administration estimated that "toddlers (2-year-olds) received 16% of their total lead exposure from food . . . 1% from soil, 7% from water, and 75% from dust." Id. at 415.
*259 ¶ 33. Lead poisoning disproportionately affects lower-income, inner-city populations. The National Health and Nutrition Examination Survey (NHANES III) (conducted from October 1991 to September 1994) indicated that BPb levels among children aged 1-5 years "were more likely to be elevated among those who were poor, non-Hispanic, black, living in large metropolitan areas, or living in older housing (with potential exposure to lead from lead-based paint)." Id. The differences in housing conditions and exposures to lead-containing house dust "appear to contribute to the racial differences in urban children's [BPb] levels." Id., 417.
¶ 34. Approximately 3 million tons of lead remain in an estimated 57 million occupied private housing units built before 1980. Preventing Lead Poisoning, 18. Of those units, 3.8 million contain children and deteriorated lead paint. Id. Although lead paint is typically found on kitchen and bathroom walls, it is also commonly found on doors, windows, and wood trim in pre-1950s homes. Id., 19.
¶ 35. As mentioned, the risk of lead poisoning is increased when the paint itself, or underlying surface on which it is painted, has deteriorated. Id. Lead paint on windows is particularly concerning "because it is abraded into dust by the repeated opening and closing of these windows." Id. However, even if it is intact, the risk of lead poisoning is greater if the lead paint is located on surfaces accessible to children. Id.
B. Lead Paint and White Lead Carbonate Pigment.
¶ 36. Paint is comprised of two major components: the pigment, which provides hiding power and protects the surface, and the vehicle, which allows the pigment to *260 be spread and adhered to a surface. In the first part of the 20th century, there were many different types of pigment, lead and non-lead based.[13] Generally, paint manufacturers decided what pigments and amounts of pigments to use when formulating their paints. Many of the Pigment Manufacturers also produced ready-mixed lead-based paint.
¶ 37. The predominant lead pigment that was manufactured and integrated into paint was white lead carbonate. White lead carbonate was the first chemical produced commercially in this country. That pigment was initially favored because when used alone it was the most durable and easy to apply. It was also believed to be a mildewcide.[14] All of the Pigment Manufacturers, or their predecessors-in-interests, produced this pigment at varying times since the houses in which Thomas resided were constructed in 1900 and 1905.
¶ 38. White lead carbonate could be comprised of any of three different chemical compounds. Basic lead carbonate had two chemical compositions, 4PbCO32Pb(OH)2PbO and 2PbCO3Pb(OH)2. Free normal lead carbonate's chemical composition was PbCO3. Basic lead carbonate was the overwhelming form of lead pigment used in paint.
¶ 39. In addition to having different chemical compositions, the physical properties of white lead carbonate varied. These variances included different *261 specific gravity,[15] bulking values, oil absorption, hiding power, and particle size and shape.[16] Pigment Manufacturers also distinguished between grades of lead carbonate and apparently promoted each for different purposes.
¶ 40. Thomas's toxicologist expert, Mushak, opines that the toxicological effects of white lead carbonate remain the same notwithstanding the formulary differences between the white lead carbonate pigments. Mushak states that there is little relationship between chemical diversity and the "bioavailability" of the lead, which refers to the lead uptake or lead absorption into the human body. Mushak explains that "[t]he reasons why one cannot automatically equate differences in chemical composition with differences in bioavailability is because bioavailability operates via a set of biological, biochemical and physico-chemical processes that will often render starting forms of lead in pigments indistinguishable in toxicokinetic terms."[17] Based on observational evidence (which Mushak characterizes as "the huge body of toxicological literature showing that lead *262 paint poisoning is pervasive and rather uniformly intense as to the severity of exposures") and laboratory evidence, Mushak concludes that there is no basis to conclude that formulary changes among white lead carbonates affect the bioavailability of the lead.
C. Knowledge of the Toxicity of Lead Pigments
¶ 41. In 1848, Samuel L. Dana, an American doctor, translated the first complete clinical description of lead poisoning based on over 1,000 cases, written by Tanquerel des Planches of France in 1839. Planches' work obtained preeminent status and was a leading authority on the dangers of lead through at least the 1920s. That treatise recognized the dangers of repeated inhalation of small quantities of lead.
¶ 42. By the turn of the 20th century, it was well-recognized that controlling lead dust could significantly reduce lead poisoning, although the recognition was initially limited to industrial settings. European countries had acknowledged the harm of lead dust, and by 1910, Germany, England, and France were already regulating lead industries to protect their workers from lead dust and fumes. That same year, in the United States at a meeting of the Superintendents of the National Lead Company, Dr. Alice Hamilton, M.D., the founder of industrial hygiene, applauded these countries' efforts and detailed the advanced protections European workers enjoyed.[18] Given the dwindling numbers of lead poisoning in those European countries that passed regulatory legislation, Hamilton called on American industries to reform their practices to mimic *263 their European counterparts. Above all, she argued, the first step was to abolish, or at least reduce to the greatest extent possible, lead dust.
¶ 43. Consistent with Hamilton's assessment, National Lead reported to its stockholders in 1912 that "[i]n the manufacture of the various products of Lead, there are two sources of danger to the health of workmen therein employed; viz., the fumes arising from the smelting or melting of metallic lead, and the dust arising in the process of making white lead and lead oxides." Seven years later, in 1919, the Chairman of National Lead Company's Manufacturing Committee described that "[t]he prime object" for safely handling white lead and other lead dust was "to keep lead dust out of the nose and mouth of the worker."
¶ 44. Other than manufacturing, Hamilton also monitored trade painters. In 1913, at the International Congress of Master Painters, Hamilton suggested that painters not use white lead paints for interior work.[19] Her suggestion was not generally followed, and, in 1919, she lamented that painting was "the most notorious of the lead trades" as "painters make up the large majority of the cases of lead poisoning." Aside from smeared paint present on the painters' hands that could be carried to the mouth, Hamilton noted that paint dust, caused primarily by rubbing old or new paint with sandpaper, "is universally recognized as the most dangerous part of the painters' trade." Hamilton's concerns were not unfounded. In 1910, a bill was introduced in Congress, in the House of Representatives, that would have required "[t]hat the introduction into any state . . . *264 of any white lead or mixed paint containing white lead which is not labeled with a skull and crossbones and the words `Poison; white lead' is hereby prohibited." That bill was defeated. Although protective regulatory legislation would have likely yielded beneficial results, "[t]he total prohibition of lead paint for use in interior work would do more than anything else to improve conditions in the painting trade," Hamilton stated.
¶ 45. The appreciation of the dangers lead paint posed inside the home to the residents was also emerging during this time. In July 1904, in its monthly publication The S.W.P., Sherwin-Williams publicized the hazards of white lead paint. Under the bold headline, "DANGERS OF WHITE LEAD," Sherwin-Williams reported that a committee in France had been appointed to investigate the use of white lead and other lead mixtures for painting houses. Sherwin-Williams noted that one of the committee's experts indicated that lead paints were "poisonous in a large degree, both for the workmen and for the inhabitants of a house painted with lead colors." Sherwin-Williams also noted that the expert was of the opinion "that the absolute disuse of white lead has become an imperative necessity." Nevertheless, six years later, in 1910, Sherwin-Williams began manufacturing white lead carbonate after it acquired a white lead processing plant. Moreover, in 1917, during the First World War, Sherwin-Williams advised the War Department that government specifications for 50 percent white lead carbonate paint for war helmets should be replaced with its lead-free lithopone pigment. Sherwin-Williams stated that the advantage of switching to its lithopone pigment was that the danger from lead poisoning was entirely eliminated.
¶ 46. In 1914, the director of the scientific section of the Paint Manufacturers' Association of the United *265 States, Henry A. Gardner, also warned of the hazards lead paint posed to residents. After detailing the efforts made to prevent workers from the hazards of lead dust in factories, Gardner asked why similar care was not being used to guard against lead dust in public buildings. Gardner observed that many tons of white leaded paint had been applied to the inside of schools and hospitals. And with white lead carbonate dust resulting from the gradual disintegration of this paint, Gardner noted that just as was the case with industrial workers, the presence of such dust in the room's atmosphere was very dangerous.
¶ 47. In 1919, the International Labour Organization held a meeting in Washington to enlist U.S. support in regulating white lead. Following this meeting was a conference in Geneva in 1921, under the auspices of the League of Nations, which was attended by 400 delegates from 40 countries.[20] That conference resulted in a recommendation that lead paint be banned altogether for interior uses.[21] Industry press reviews in the United States viewed the recommendation as a sinister plot by labor interests. The industry press reviews happily reported that there was little danger of any bans on lead paint in the United States.
¶ 48. In 1939, the National Paint Varnish and Lacquer Association (NPVLA) confidentially warned its memberswhich included National Lead, Sherwin Williams, Glidden, and W.P. Fullerthat white lead pigments *266 were toxic. This letter, marked "CONFIDENTIAL Not for Publication," stated:
[T]he vital factor concerning toxic materials is to intelligently safeguard the public. People may feel safer in buying materials whose danger they know rather than materials unknown to them.
. . . .
The following pigments may be considered toxic if they find their way into the stomach. . . .
. . . .
Lead Compounds. White lead, red lead, litharge, lead chromates (chrome yellow, chrome green), or other lead pigments.
The letter proceeds to explain that the NPVLA expected that manufacturers would apply "every precautionary measure in manufacturing, in selling and in use where toxic materials are likely to or do enter a product." The letter noted that "children's toys, equipment, furniture, etc. are not the only consideration." It also contained the following notification of legal duties to warn of a dangerous product:
1. A manufacturer who puts out a dangerous article or substance without accompanying it with a warning as to its dangerous properties is ordinarily liable for any damage which results from such failure to warn.
. . . .
9. The manufacturer . . . must know the qualities of his product and cannot escape liability on the ground that he did not know it to be dangerous.
10. The general rule that a manufacturer is not liable to those not in privity of contract with him does not apply when his product is imminently or inherently dangerous.
*267 ¶ 49. Nevertheless, the NPVLA fought to weaken states' proposals that required paint to contain warning labels and particularly objected to the American Medical Association's proposal that would have required lead paint to be labeled as "poisonous."
¶ 50. By 1942, the National Safety Council determined that "the most obvious method of preventing lead poisoning is to substitute for lead and its compounds other materials that are non-toxic." By the early 1920s, there were safe alternatives to white lead paint. During that time, Glidden and Sherwin-Williams produced zinc-based paints, while National Lead pioneered the development of titanium pigments. These pigments were being manufactured and marketed particularly because of the appreciation of lead's toxicity.[22]
¶ 51. As noted above, during World War I, Sherwin-Williams advised the War Department to switch its order for helmets with 50 percent lead carbonate paint to Sherwin-Williams' lead-free lithopone paint in order to eliminate the prospect of lead poisoning. Glidden promoted its lead-free paints by claiming: "Lead Paints are banned in Europe because of the danger of Lead Poisoning. [Titan-O-Zinc] is lead-free, consequently, non-poisonous. Not only is it ideal for residence painting and every other exterior surface, but the attention of the farmer is especially called to this product as it eliminates all possibility of lead poisoning of livestock characteristically known as `cribbers.'"
¶ 52. Although various manufacturers of zinc-based paints published ads attacking lead paints as poisonous, National Lead silenced those advertisements by reaching an agreement with zinc pigment *268 manufacturers to refrain from attack ads sometime between 1905 and 1918. By 1928, National Lead was one of the leaders in the production of titanium pigments. After the Second World War, even though National Lead was producing lead-free paints, it advised its salespeople to push the sale of leaded paints "at every opportunity."
D. Knowledge of Childhood Lead Poisoning
¶ 53. Parallel with the emerging knowledge of the dangers caused by lead in industrial and residential settings grew the awareness of childhood lead poisoning. During the mid-1800s, child lead poisoning was already linked to mouthing lead-painted toys. Australia was at the forefront of identifying and examining childhood lead poisoning. Following the first well-documented study of childhood lead poisoning from paint in 1908, Australian researchers went so far as to call for prohibiting the use of lead paint within the reach of children. They found:
Two conditions of painted surfaces would be more than usually liable to induce poisoning, viz., (a) freshly painted or at least sticky surfaces; (b) painted surfaces which have either been exposed to the sun and air, and whose paint has lost its oil and become a dry easily detachable powder, or which though not exposed have lost some of their oil and gloss, and which when rubbed yield a powdery substance to the touch and possibly distribute it to the dust of rooms.
¶ 54. During that same year, Australian researchers also connected paint powder stuck to children's fingers, which were then bit or sucked, with lead poisoning. Those researchers also recommended refraining from using lead paint on surfaces accessible to children.
*269 ¶ 55. In the early 1900s, children's particular susceptibility to lead poisoning was also gaining recognition. In Great Britain, the dangers of lead exposure to fetuses were identified, and women were later removed from working in the lead industries. In the United States, in 1908, Dr. Hamilton noted that "lead is a most potent producer of abortion, and it is very rare that a woman lead worker bears a healthy child at term." And, in 1912, researchers in the United States acknowledged that young people were more vulnerable to lead poisoning than adults. In its 1912 annual report, National Lead noted that it did not employ women in its factories, except as occasional messengers or other similar jobs, or boys.
¶ 56. In 1914, a physician from John Hopkins Hospital who was also professor at the John Hopkins Medical School, Dr. Kenneth D. Blackfan, chronicled a case of a five-year-old boy from Baltimore w