Lead, human exposure measurements

The absorption, distribution, and accumulation of lead in the human body may be represented by a three-part model (6). The first part consists of red blood cells, which move the lead to the other two parts, soft tissue and bone. The blood cells and soft tissue, represented by the liver and kidney, constitute the mobile part of the lead body burden, which can fluctuate depending on the length of exposure to the pollutant. Lead accumulation over a long period of time occurs in the bones, which store up to 95% of the total body burden. However, the lead in soft tissue represents a potentially greater toxicological hazard and is the more important component of the lead body burden. Lead measured in the urine has been found to be a good index of the amount of mobile lead in the body. The majority of lead is eliminated from the body in the urine and feces, with smaller amounts removed by sweat, hair, and nails. 

Flegal AR, Smith DR. 1995. Measurements of environmental lead contamination and human exposure. Rev Environ Contam Toxicol 143 1-45. 

Effect of Dose and Duration of Exposure on Toxicity. No studies were located where -hexane concentration was measured in workplace air before workers became ill, so no dose-response relationship can be defined for human neurotoxicity as the result of -hexane exposure. Information on duration of exposure leading to toxicity is available from some case series reports. An occupational exposure caused sensory disturbances in the lower extremities after approximately 2 months (Herskowitz et al. 1971). A case of peripheral neuropathy after 7 months of exposure was reported among press-proofing workers in Taipei (Wang et al. 1986) a serious case resulting in quadriplegia after 8 months of exposure was reported among sandal workers in Japan (Yamamura 1969). Based on case reports, it can be estimated... 

At the beginning of this book, we presented some discussion of health-based air quality standards. In the final chapter, which follows this one, the scientific bases of control measures for various pollutants are discussed. In between, the complex chemistry that occurs in both polluted and remote atmospheres, and that converts the primary pollutants into a host of secondary species, has been detailed. To provide further perspective on airborne gases and particles and human exposure levels, we briefly treat indoor air pollution in this chapter. As we shall see, for many species it is simply a question of emissions leading to elevated levels indoors. However, there is some chemistry that occurs in indoor atmospheres as well, and it is of interest to compare this to that occurring outdoors. 

Numerous sources of ionizing radiation can lead to human exposure natural sources, nuclear explosions, nuclear power generation, use of radiation in medical, industrial and research purposes and radiation-emitting consumer products. Before assessing the radiation dose to the population, one requires a precise knowledge of the activity of a number of radionuclides. The basis for the assessment of the dose to the population from a release of radioactivity to the environment, the estimation of the potential clinical health effects due to the dose received and, ultimately, the implementation of countermeasures to protect the population is the measurement of radioactive contamination in the environment after the release. The types of radiation one should consider include ... 

The potential for unusual health effects of chemical mixtures due to the interaction of chemicals or their metabolites (e.g., metabolites of trichloroethylene and benzene) in or with the biosystem constitutes a real issue in the public health arena. However, toxicity testing to predict effects on humans has traditionally studied one chemical at a time for various reasons convenient to handle, physiochemical properties readily defined, dosage could easily be controlled, biologic fate could easily be measured, and relevant data were often available from human occupational exposures. Chemicals are known to cause disease for example, arsenic and skin cancer, asbestos and lung cancer, lead and decrements of IQ, and hepatitis B predisposes to aflatoxin-induced liver cancer but the link between the extent of human exposure to even well-defined chemical mixtures and disease formation remains relatively unexplored, but of paramount importance to public health. 

The term reduction means measures designed to reduce or eliminate human exposure to lead-based paint hazards through methods including interim controls and abatement. 

For measuring lead in environmental media providing potential human lead exposures, this chapter includes older published data for lead concentrations in media, data which are old enough to encompass the full lifetimes of living populations. This is because of long-term Pb storage in bone. One concern with any appraisal of older lead measurement data in media is that of analytical and statistical data reliability versus that of methods employed with more recent accepted techniques. Sensitivity is of particular concern. A potent toxicant such as environmental lead requires methods for quantification of concentrations of lead at ultra-trace levels in order to permit estimates of the full range of Pb exposures. 

There are a variety of field and laboratory analytical methods for soil lead measurement, depending on the type of analysis and its purposes in a given evaluation. Bulk soil lead measurement refers to measurement of the total lead content of the soil sample. Chemical speciation and micromineralogical studies in the context of human lead exposure variability refer to amounts of specific chemical forms of lead and their geochemical states. These studies are sometimes done in tandem with relative bioavailability testings, i.e., amounts of lead being absorbed under in vivo or in vitro simulation of in vivo conditions (Casteel et al., 2006) with respect to Pb source attribution. Stable isotopic analysis studies deal with the quantitative stratification of lead s stable isotopic composition into the four main stable isotopes lead-204, lead-206, lead-207, and lead-208 (Gulson et al., 1995, 1997). 

Concentrations of lead in the various environmental media described in this section are presented for extended periods. The available data that meet minimal statistical and measurement criteria generally only extend from the late 1960s/early 1970s to the present. The purposes of a wide temporal look at environmental lead concentrations are several. First, the nature of lead as an accumulating contaminant in the bodies of human populations requires an appreciation of the amounts of environmental lead that existed in past decades. As noted earlier, lead levels in media have been changing, mainly downward, so that current human body lead burdens are only partially quantifiable from current lead intakes into body compartments. Secondly, the use of predictive, biokinetic models of human lead exposures for simulating Ufe-time lead exposures requires knowledge of lead intakes from the earliest periods of life. 

National and International Dietary Pb Surveys A number of dietary Pb surveys have been carried out in the United States and around the world. Summaries of these surveys are presented in this section. Some surveys have simply reported descriptive statistics for lead concentrations in dietary groups and levels of Pb in individual food components within those groups, e.g., measured Pb levels in cereals as a group. Other surveys have reported Pb levels in dietary components and coupled these with consumption patterns to provide intakes of food Pb in some time frame, typically as daily total intakes. Some survey reports have mainly concerned themselves with total dietary Pb intakes. This chapter confines itself to Pb levels in foods and presents intakes and uptakes in the context of human exposures in later sections. 

A number of more recent studies indicate that Pb appears to function as a disrupter of endocrine action, based on data from both male and female animals and results of studies in male Pb workers. The nature and extent of such disruptions, however, are not consistent. The search for endpoints in human populations has measured levels of various hormones in accessible biological media, such as serum or plasma, obtained from mainly smelter or lead battery plant employees. PbB levels have ranged considerably across these investigations (Table 19.2), with typically observed mean or median PbB values of 30—40 pg/dl. These studies complement, at a lower part of the dose—response curve, the earlier findings of Braunstein et al. (1978) and Cullen et al. (1984) where Pb exposures were much greater, sufficient to produce clinical evidence of lead poisoning. 

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