Occupation exposures, lead

Chronic Occupational Exposure Lead is the most widely used nonferrous metal, and a large number of occupations may be associated with risk of exposure. 

Because of the toxicity of lead, special care must be taken when working with lead ahoys. Lead and its inorganic compounds are neurotoxias which may produce peripheral neuropathy. Eor an overview of the effects of lead exposure, see Occupational Exposure to Lead, Appendix A (29 CRE 1910.1025) (see... 

See pubhcations of R. LiUs for additional studies related to the toxicity of lead following occupational exposure. These pubHcations have been compiled into a volume entitied Studies on Eead Exposed Occupational Groups 1967—1989 and ate available from the Dept, of Community Medicine, Mount Sinai School of Medicine, New York, 1991. 

Comparison of the results of the occupational exposure concentration with the OEL leads to three different possibilities. 

Less than 0.5 percent of the black children at the Dixie site were found to have lead toxicity (Table XX). As previously noted, the three non-black children (6.6 percent of non-black children) found to have lead toxicity were siblings In a household where the father had an occupational exposure to 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. 

Increases in ALAS activity have been observed in lead workers (Meredith et al. 1978). Leukocyte ALAS was stimulated at a PbB level of 87 pg/dL (Meredith et al. 1978), a level at which ALAD activity is already significantly inhibited. ALAD activity correlated inversely with PbB levels in occupationally exposed individuals (Alessio et al. 1976 Wada et al. 1973), as has been seen in subjects with no occupational exposure (Secchi et al. 1974). Erythrocyte ALAD and hepatic ALAD activities were correlated directly with each other and correlated inversely with PbB levels in the range of 12-56 pg/dL (Secchi etal. 1974). 

Histopathological evidence of renal damage has been observed in lead-exposed workers. Renal ultrastructure and function were examined in five men with heavy occupational exposure to lead (Cramer et al. 1974). In addition, renal function was evaluated in two men from whom renal biopsies were not obtained. PbB levels ranged from 71 to 138 pg/dL. Renal function tests were normal in all except for a reduced glomerular filtration rate in one worker. Two subjects with relatively short exposure to lead (6 weeks and 8 months) and PbB levels of 89-129 pg/dL had intranuclear inclusions in the proximal tubules. Renal biopsies from workers with longer periods of lead exposure (4-20 years, PbB levels of 71-138 pg/dL) had diffuse interstitial or peritubular fibrosis. Glomeruli were normal in all subjects. 

Selected studies are discussed below and include reports on occupational exposure to lead for females and males followed by environmental (low level) exposure to lead in females and males. 

Chowdhury et al. (1986) reported that occupational exposure of 10 men to lead caused a significant decrease in sperm count and motility and an increased percentage of abnormal spermatozoa. The average PbB concentration in the lead-exposed group was higher (42.5 pg/dL) compared to controls (14.8 pg/dL). Assennato et al. (1987) reported decreased sperm production in 39 battery factory workers with high PbB levels ranging from 50 to 61 pg/dL, compared to 39 nonexposed workers. Lerda (1992)... 

The information available regarding the association of occupational exposure to lead with increased cancer risk is generally limited in its usefulness because the actual compound(s) of lead, the route(s) of exposure, and level(s) of lead to which the workers were exposed were often not reported. Furthermore, potential for exposure to other chemicals including arsenic, cadmium, and antimony occurred, particularly in lead smelters, and smoking was a possible confounder (Cooper 1976 IARC 1987). These studies, therefore, are not sufficient to determine the carcinogenicity of lead in humans, and the following discussion is restricted to the most comprehensive of these studies. 

Deaths associated with occupational exposure to inorganic lead (which is predominantly by the inhalation route of exposure) are discussed in Section 2.2.1.1. No studies were located regarding death in animals after inhalation exposure to inorganic lead. 

Musculoskeletal Effects. Individuals who have had high exposures to lead, either occupationally or by the consumption of alcohol from lead stills, have been reported to exhibit a bluish-tinged line in the gums (i.e., the "lead line"). In addition, case reports of high occupational exposure to lead have described the occurrence of muscle weakness, cramps, and joint pain. 

Reproductive Effects. There is sufficient qualitative evidence to support the conclusion that at high occupational exposure levels lead has significant adverse effects on human reproduction, including increased incidences of spontaneous abortion, miscarriages, and stillbirths. The mechanisms responsible for these effects are unknown at this time, but many factors may contribute to these results. These factors include indirect effects of lead on maternal nutrition or hormonal status before and during pregnancy to... 

Results from a recent study showed a marginally significant association of Parkinson s disease with more than 20 years of occupational exposure to lead (Gorell et al. 1997) when the analysis included more than 20 years of combined exposure to lead and iron, the association greatly increased, with the odds ratios exceeding that for exposure to one of the metals alone. 

Information on occupational exposure to lead is obtained primarily from the National Occupational Exposure Survey (NOES) and industry surveys of workers. While occupational exposure is widespread, environmental monitoring data on levels of exposure in many occupations are not available. OSHA has established a permissible exposure limit (PEL) for lead of 50 pg/m3 for workplace air (OSHA 1991). NIOSH has estimated that more than 1 million American workers were occupationally exposed to inorganic lead in more than 100 occupations (NIOSH 1977a, 1978a). According to NOES, conducted by NIOSH between 1980 and 1983, an estimated 25,169 employees were exposed to tetraethyl lead (not used in gasoline since December 31, 1995) approximately 57,000 employees were exposed to various lead oxides mostly in non-ferrous foundries, lead smelters, and battery plants 3,902 employees were exposed to lead chloride and 576,579 employees were exposed to some other form of lead in the workplace in 1980 (NIOSH 1990). Workers who operate and maintain solid waste incinerators are also exposed to air lead levels as high as 2,500 pg/m3 (Malkin 1992). 

OSHA requires employers of workers who are occupationally exposed to a toxic or hazardous substance to institute engineering controls and work practices that maintain or reduce their exposure to a level that is at or below the permissible exposure limit (PEL) established for the substance. For occupational exposures to lead, the employer must use engineering controls and work practices to achieve an occupational exposure of 50 pg/nr3 (0.006 ppm) or lower, based on an 8-hour time-weighted average (TWA) (OSHA 1995). When employee exposures to lead can not be maintained at or below 50 pg/rn3... 

Christoffersson JO, Ahlgren L, Schutz A, et al. 1986. Decrease of skeletal lead levels in man after end of occupational exposure. Arch Environ Health 41 312-318. 

Cocco PL, Cocco E, Anni MS, et al. 1991. Occupational exposure to lead and blood cholesterol in glucose-6-phosphate dehydrogenase deficient and normal subjects. Res Commun Chem Pathol Pharmacol 72(1) 81-95. 

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