Human exposure to lead and its effects

There is a long history of human exposure to lead, although the relative importance of the different pathways of lead intake may have altered over recent decades. Widespread use was made of lead during the time of the Roman Empire such uses included the lining of aqueducts and the fabrication of water pipes and cooking utensils, [1]. It is likely that both food and drink will have been substantially contaminated with lead and adverse health effects may have resulted. 

Although the toxic effects of metals have merited considerable attention, it should be recognized that many metals also have an essential role to play in biological systems.There is some recent tentative evidence that lead may display this dual role of essentiality and toxicity [2]. Nevertheless, at the concentrations to which the human population is exposed it is reasonable to be concerned principally with the prevention of adverse effects resulting from excessive exposure, rather than the avoidance of possible deficiency syndromes. In this context, it is necessary to have regard to the various sources of human exposure, the intake from these sources, the subsequent uptake and metabolism of the lead in the body and finally, to the adverse effects. These matters will be dealt with separately in the following sections. 

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Human exposure to lead and its effects 141 7.3 Uptake of lead... 

As discussed in the introduction to Section 2.2, the bulk of the human data on the health effects of lead are expressed in terms of internal exposure, or PbB levels, rather than external exposure levels (i.e., mg/m3 or mg/kg/day). For the general population, exposure to lead occurs primarily via the oral route with some contribution from the inhalation route, whereas occupational exposure is primarily by inhalation with some oral. Therefore, it is difficult to distinguish specific routes and levels of exposure. For this reason, the human health effects data for lead will be presented in terms of PbB levels in this section. Health effects associated with human exposures to lead and internal lead doses are shown in Table 2-1. 

In the previous sections an attempt has been made to define the major pathways of human exposure to lead and then to examine the resultant blood lead concentration as a biological indicator of this exposure. It thus follows that the biological effects should, in so far as possible, be likewise related to this same index of exposure, the blood lead concentration. Furthermore, it is this mobile lead in the bloodstream that is the cause of the adverse effects of lead. 

Respiratory Effects. The only information located regarding respiratory effects in humans associated with lead exposure was a case report of a 41-year-old man who was exposed to lead for 6 years while removing old lead-based paint from a bridge. At the time of the initial assessment, his PbB level was 87 pg/dL, and he complained of mild dyspnea for the last 2-3 years. No abnormalities in respiratory function were seen at clinical examination, so it is not possible to conclude that his respiratory symptoms were related to exposure to lead (Pollock and Ibels 1986). 

Ferguson and Bowman 1990 Gilbert and Rice 1987 Hopper et al. 1986 Krasovskii et al. 1979 Levin et al. 1988 Massaro and Massaro 1987 Overmann 1977 Rice 1985a). It appears that animals are affected at roughly the same blood lead levels as humans. Measured neurotoxic effects in animals include significantly delayed motor function and reflexes, decreased performance on learning tasks, and impaired spatial discrimination. Additional animal studies are needed to investigate the neurotoxic effects of subchronic inhalation exposures to establish external dose-effect relationships. 

Sherlock JC, Ashby D, Delves HT, et al. 1984. Reduction in exposure to lead from drinking water and its effect on blood lead concentrations. Human Toxicol 3 383-392. 

On contact with moist membranes, S02 forms sulfurous acid, which is responsible for its severe irritant effects on the eyes, mucous membranes, and skin. It is estimated that approximately 90% of inhaled S02 is absorbed in the upper respiratory tract, the site of its principal effect. The inhalation of S02 causes bronchial constriction altered smooth muscle tone and parasympathetic reflexes appear to be involved in this reaction. Exposure to 5 ppm for 10 minutes leads to increased resistance to airflow in most humans. Exposures to 5-10 ppm are reported to cause severe bronchospasm 10-20% of the healthy young adult population is estimated to be reactive to even lower concentrations. The phenomenon of adaptation to irritating concentrations is a recognized occurrence in workers. Asthmatic individuals are especially sensitive to S02. 

The most probable cause of a submarine sinking is flooding caused by an event that breaches the outer hull. The force required would have to be substantial. Potential causes include surface collision, grounding, external explosion, and catastrophic failure of a hull valve. It is likely that such an event also would start a fire within the submarine. The immediate concern for the crew is the release of toxic gases that are produced as the combustion products of on-board fires (U.S. Navy 1998). Human exposure to these gases can lead to adverse health effects, particularly respiratory and central nervous system effects, and even... 

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