Timeline on the Toxicology of Lead

200 B.C. Nicander recognized lead poisoning paralysis. (Hunter, 1974 p240)

100 AD Dioscorides described lead colic, paralysis and delerium from the ingestion of lead or the inhalation of lead fumes. Mechanical devices used to reduce exposure. (Hamilton and Hardy 1949 p49; Hunter 1974 p240)

1656 Outbreaks of lead poisoning in France from its use in wine making. Notorious outbreaks of lead poisoning from widespread use of lead in cooking vessels and other household articles. (Stockhousen 1656 cited in Hamilton and Hardy 1949 p49)

*1785 Lead in pottery glazes called "a slow but sure poison" sometimes poisoning whole families in early America. (McCord 1954 p78)

1839 Tanquerel des Planches published in Paris his work on 1,200 cases of occupational lead poisoning in numerous trades. (Hunter, 1975 p238, 240; Hamilton and Hardy 1949 p49)

1878 Children and young persons excluded from the manufacture of white lead under the Consolidating Act of 1878. (Hunter, 1975 p238, 240)

1883 The first Act of Parliment to be directed against a specific occupational disease was the Factories (Prevention of Lead Poisoning) Act of 1883. (Hunter, 1974 p238, 240)

1895 The dangers of lead in plumbing were recognized. (Remington, 1895)

1892 Lead poisoning was found in children in the Brisbane area of Australia. Chalking lead-based paint in homes was identified as the source of the poisoning in 1904. (Gibson 1892, 1904; cited in Hammond and Dietrich 1990 p91-92)

1900 In Great Britain, 1,058 cases of occupational lead poisoning were reported in the year 1900. 7,936 cases including 328 fatalities in the years 1900-1911. (Hunter, 1974 p241; Glaister 1938 p590)

1910 High rates of lead poisoining in pottery workers in the U.S. (Hamilton and Hardy 1949 p58)

1912 Miscarriage rates found to be higher in women exposed to lead at work. (Legge & Goadby 1912 cited in Bartrop 1969)

1914 Childhood lead poisoning from lead house paints was identified in the United States. (Thomas and Blackfan 1914 cited in Hammond and Dietrich 1990 p91-92)

1914 Widespread lead poisoning of women and children living in a smelter village in Mexico. (Hall 1914 cited in Hamilton and Hardy 1949 p102)

1914 Livestock poisoning around the Selby smelter. Asarco's Department of Agricultural Research formed to monitor pollution and resolve claims against Asarco. (Haring and Meyer 1915 as cited in Aronson 1972)

1922 132 cases of lead encephalopathy amongst workers in American lead industries in years 1910-1922. Many left with permanent mental deterioration, blindness or paralysis. (Hamilton and Hardy 1949 p80)

1922 428 cases of severe lead poisoning in children of Queensland, Australia traced to white lead paint on the verandas where the children play. (Gibson, 1922 cited in Hamilton and Hardy 1949 p73; and Hunter 1974 p257, 264)

1929 Nye reported impaired growth in overtly lead-poisoned children. (ATSDR 1993 p34)

1933 Brain damage in children following lead poisoning. (McKhann and Vogt 1933 cited in Cumings 1959 p104)

1938 Acute encephalopathy occurs in the most susceptible children at blood lead levels in the range of 80-100 ug/dl. (Gant 1938; Bradley and Baumgartner 1958; Bradley et al. 1956 cited in ATSDR 1992 p41)

1941 U.S. Public Health Service set occupational exposure standard for lead at 1.5 mg per 10 cubic meters. (Hamilton and Hardy 1949 p60)

1942 Lead poisoning in U.S. miners. (Hamilton and Hardy 1949 p58)

1943 Mild lead poisoning in infancy found to cause permanent brain damage in children evident as learning and behavioral disabilities. Pica in children is noted. (Byers and Lord 1943 cited in Baloh 1973)

1950 Continued reports of livestock poisonings from smelter emissions. (Allcroft and Blaxter 1950 as cited in Barltrop et al. 1973; Aronson 1972)

1954 The majority of instances of mild lead poisoning are never recognized by physicians. (McCord 1954 p123)

1965 Patterson notes residents of the United States today are undergoing severe chronic lead insult. Even mild lead absorption will produce significant amounts of intellectual irritability and dysfunction. (Patterson 1965).

1966 Lead exposures of epidemic proportions in children near lead smelters. (Oyanguren and Perez 1966 cited in Popovac, 1982 p22)

1968 General agreement that any increase in the body burden of lead is undesirable. (Stern 1968 p602)

1969 Lead poisoning called the "silent epidemic" by American Academy of Pediatrics. (Alpert and Breault 1969 as cited in Mausner and Kramer, 1985 p36)

1970 Lead poisoning due to soil ingestion had been reported. (Orton, 1970 as cited in Barltrop et al., 1973)

1970 Blood lead level of 16 ug/dl was found to cause fifty percent inhibition erythrocytic ALAD activity. (Hernberg and Nikkanen 1970 cited in Hammond and Dietrich 1990)

1972 Lead poisoning epidemic in children living near the Asarco lead smelter in El Paso, Texas. Significantly lower intelligence scores were found in these children by 1975. (Landrigan et al., 1975 cited in Popovac, 1982 p22)

1972 Neuropsychological deficits found in preschool children exhibiting pica for paint and plaster and elevated blood lead levels (>40 ug/dl, mean 58 ug/dl). (de la Burde and Choate 1972 cited in ATSDR 1992 p41-42)

1972 Hyperactivity in children was associated with higher blood lead levels and post-penicillamine urine lead levels. Blood lead levels in the "pure" hyperactive group averaged 26.23 ug/dl. "Our findings suggest that the arguments for considering any lead elevation above 24.5 ug/dl as dangerous should receive serious attention. (David et al. 1972; see also Needleman, 1973; cited in Feldman et al. 1980)

1973 Prevalence of pica is high in children aged 2-3 years. (Bartrop et al. 1973)

1974 Ingestion of dirt and dust shown to be the major route of lead absorption by children. (Angle et al. 1974; Roberts et al. 1974 cited in Roels et al 1980)

1975 Neuropsychological deficits and failure in school due to learning and behavior problems noted in 7-year-old children who had asymptomatic lead exposure between 1 and 3 years of age. Blood lead values at age 1-3 years were >40 ug/dl (mean 58 ug/dl). (de la Burde and Choate 1975 cited in ATSDR 1992 p41-42)

1976 Effects on the peripheral nervous system found in children aged 5-9 yrs exposed to lead from smelters in Kellogg, Idaho. (Landrigan et al., 1976 cited in Landau et al. 1977)

1979 Lead shown to cause IQ deficits and other neurobehavioral defects in children. (Needleman et al. 1979 as cited in ATSDR 1993 p43)

1986 Prenatal lead exposure associated with lower birth weight, shorter gestation, minor anomalies, and neurobehavioral deficits. (citations in Dietrich et al. 1987)

1987 No threshold found for the adverse effect of lead on IQ. Dose-response effect down through the lowest exposure groups (~6 ug/dl). (Fulton et al. 1987; Silva et al. 1988; cited in ATSDR 1993 p44-46)

1987 Lowered performance on neuropsychological tests found in children with prenatal blood levels in the range of 10-25 ug/dl. Indications of this effect in infants whose cord blood levels were 6-7 ug/dl (mean 6.5 ug/dl) as compared to <3 ug/dl (mean 1.8 ug/dl) controls. (Bellinger et al. 1987 cited in Smith and Flegal 1992)

1988 Neuropsychological deficits in children at age four living down wind of the lead smelter in Port Pirie, Australia. Children's blood lead levels in the range of 6.21-41.4 ug/dl. A blood lead increase from 10.3 ug/dl to 31 ug/dl was estimated to result in an additional 15% of children considered to have developmental delay requiring clinical intervention. There was no evidence of a threshold for the adverse effects of lead. (McMichael et al. 1988p)

1991 Deficits in neurobehavioral development at age 57 months associated with elevated blood lead levels at age 24 months (average 6.8 micrograms/dl. (Bellinger et al. 1991, cited in ATSDR 1992 p50)

---

ABOUT THE AUTHOR: David H. Monroe, MSPH, Ph.D.
Dr. Monroe is a toxicologist with over 20 years experience consulting in environmental toxicology, human/ecological risk assessment, and occupational/public health. As an expert witness in state and federal courts, he has provided expert testimony on the health and environmental impacts of hazardous waste sites, industrial chemicals, pesticides, groundwater contamination, indoor air pollution, contaminated sediments, lead, arsenic, mercury, and other metals. Professional positions include subject matter expert (occupational toxicology) with the Office of the Air Force Surgeon General, toxicologist with the California Department of Toxic Substances Control, and toxicologist with the U.S. Environmental Protection Agency Superfund program. His graduate studies were at the University of Washington School of Public Health and Community Medicine, where he received a Master of Science in Public Health and a Ph.D. in Environmental Toxicology.

Copyright Monroe Toxicology

Disclaimer: While every effort has been made to ensure the accuracy of this publication, it is not intended to provide legal advice as individual situations will differ and should be discussed with an expert and/or lawyer.For specific technical or legal advice on the information provided and related topics, please contact the author.