Lead
Aside from smoke, lead is probably the oldest human-made atmospheric and occupational toxin, dating back at least 8,000 years to the first lead-smelting furnaces [179]. Today, lead poisoning remains the single most significant preventable disease associated with an environmental and occupational toxin [180].
The risks of lead exposure vary greatly depending upon where one lives. In Bangkok, Mexico City, and Jakarta, exposure largely stems from automotive exhausts; however, in inner-city Chicago and Washington, D.C., exposure is mostly associated with lead in house paint [181]. Generally, human exposure to lead comes from the following main sources: using leaded gasoline; using lead-based paint; having lead pipes in water supply systems; and exposure to industrial sources from processes such as lead mining, smelting, and coal combustion. Additional sources of lead include soldered seams in food cans, ceramic glazes, batteries, and cosmetics [182].
Lead is particularly toxic to the brain, kidneys, reproductive system, and cardiovascular system. Exposures can cause impairments in intellectual functioning, kidney damage, infertility, miscarriage, and hypertension [183]. Lead is a special hazard for young children. Several studies have shown that lead exposures can significantly reduce the IQ of school-aged children; some estimates suggest that every 10-microgram-per-deciliter increase in lead levels in the blood is associated with a 1- to 5-point decrease in the IQ of exposed children [184]. Lead exposures have also been associated with aggressive behavior, delinquency, and attention disorders in boys between the ages of 7 and 11 [185]. In adults, lead exposure has been related to increased blood pressure and hypertension, conditions known to increase the risk of cardiovascular disease.
Unlike most chemicals for which health impacts of low-level doses are still uncertain, exposure to lead, even at very low levels, is highly toxic [186]. Although 10 micrograms of lead per 1 deciliter of blood is generally used as the level above which health impacts are known to be substantial, scientists have not yet identified a level below which no adverse effects of lead occur [187] [188]. Several studies have found detectable learning problems in children whose blood lead levels are as low as 5 to 10 micrograms per deciliter [189].
Exposures to unhealthy levels of lead remain common throughout both developed and developing countries. (See Lead Pollution Poses a Special Hazard to Children
.) Among urban children in developing countries, the majority of children younger than 2 years of age have average blood lead levels greater than 10 micrograms per deciliter, estimates suggest [190]. A review of 17 studies from different parts of China found that between 65 and 99.5 percent of children living in industrial and heavy traffic areas had blood lead levels above 10 micrograms per deciliter. Even outside of those high-risk areas, as many as 50 percent of China’s children had unacceptably high blood lead levels [191]. Even in Africa, despite comparatively low levels of industrialization and car usage, lead exposure is a serious problem. In Nigeria, for instance, it is estimated that 15 to 30 percent of the children in urban areas have blood lead levels greater than 25 micrograms per deciliter [192]The health toll of lead exposure is particularly high among poor populations of developed and developing countries alike, both because exposures are typically higher and because the populations may be more susceptible. In urban areas, for instance, the poor may live near major roadways where exposure to vehicle emissions is high. They also tend to live in older housing, where the risks from lead-based paint are greater. In addition, lead is believed to be absorbed from the stomach more completely when the stomach is empty and when the diet lacks essential trace elements, such as iron, calcium, and zinc [193].
References and notes
179. Josef Elsinger, “Sweet Poison,” Natural History, Vol. 105, No. 7 (July 1996), p. 50.
180. Ellen Silbergeld and Kevin Tonat, “Investing in Prevention: Opportunities to Prevent Disease and Reduce Health Care Costs By Identifying Environmental and Occupational Causes of Noncancer Disease,” Toxicology and Industrial Health, Vol 10, No. 6 (1994), p. 677.
181. A.J. McMichael, Planetary Overload: Global Environmental Change and the Health of the Human Species, (Cambridge University Press, Cambridge, 1993) p. 279.
182. Ellen K. Silbergeld, “The International Dimensions of Lead Exposure,” International Journal of Occupational and Environmental Health, Vol. 1, No. 4 (Oct./Dec. 1995), pp 338, 340.
183. Ellen Silbergeld, “The Elimination of Lead from Gasoline: Impacts of Lead in Gasoline on Human Health, and the Costs and Benefits of Eliminating Lead Additives,” draft paper (The World Bank, Washington, D.C., 1996), p. 3.
184. Robert A. Goyer, “Results of Lead Research: Prenatal Exposure and Neurological Consequences,” Environmental Health Perspectives, Vol. 104, No. 10 (October 1996), p. 1050.
185. Herbert L. Needleman et al., “Bone Lead Levels and Delinquent Behavior,” Journal of the American Medical Association, Vol. 275, No. 5 (February 7, 1996), pp. 363 -369.
186. Op. cit. 182, p. 336.
187. J. Schwartz, “Low Level Lead Exposure and Children”s IQ: A Meta-Analysis and Search for a Threshold,” Environmental Research, Vol. 65, No. 1 (1994), pp. 42-55.
188. Op. cit. 183.
189. Op. cit. 183.
190. Alliance to End Childhood Lead Poisoning (Alliance) and the Environmental Defense Fund (EDF), The Global Dimensions of Lead Poisoning: An Initial Analysis (Alliance and EDF, Washington, D.C., 1994), p. 35.
191. “Preventing Lead Poisoning in China,” Environmental Health Perspectives, Vol. 104, No. 10 (October 1996), p. 1025.
192. Jerome O. Nriagu, Mary L. Blankson, and Kwamena Ocran, “Childhood Lead Poisoning in Africa: A Growing Public Health Problem” The Science of the Total Environment, Vol. 181 (1996), p. 99.
193. Robert A. Goyer, “Results of Lead Research: Prenatal Exposure and Neurological Consequences,” Environmental Health Perspectives, Vol. 104, No. 10 (October 1996), p. 1051.
