Lead toxicity occupational exposures

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. 

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... 

Reviews on the occurrence, biochemical basis, and treatment of lead toxicity in children (11) and workers (3,12,13) have been pubhshed. Approximately 17% of all preschool children in the United States have blood lead levels >10 //g/dL. In inner city, low income minority children the prevalence of blood lead levels >10 //g/dL is 68%. It has been estimated that over two million American workers are at risk of exposure to lead as a result of their work. PubHc health surveillance data document that each year thousands of American workers occupationally exposed to lead develop signs and symptoms indicative of... 

Workers in the metals treatment industry are exposed to fumes, dusts, and mists containing metals and metal compounds, as well as to various chemicals from sources such as grinding wheels and lubricants. Exposure can be by inhalation, ingestion, or skin contact. Historically, metal toxicology was concerned with overt effects such as abdominal coHc from lead toxicity. Because of the occupational health and safety standards of the 1990s such effects are rare. Subtie, chronic, or long-term effects of metals treatment exposure are under study. An index to safety precautions for various metal treatment processes is available (6). As additional information is gained, standards are adjusted. 

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. 

When the Dixie site is compared to the reference area, proximity to the smelter (within 0.5 mile) contributed 1.85 pg/dl to the mean blood-lead level. The potential contribution of traffic density could not be determined because of the configuration of the roadway and the distance of the roadway from the smelter site. Although an elevated mean blood-lead level was found for children living close to the Dixie site, the increase was not as great as observed in the RSR site and the few children found to have lead toxicity, as defined previously, appear to have lead exposure due to occupation of parents. 

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... 

Raghavan SRV, Culver BD, Gonick HC. 1980. Erythrocyte lead-binding protein after occupational exposure I. Relationship to lead toxicity. Environ Res 22 264-270. 

Somashekaraiah BV, Venkaiah B, Prasad ARK. 1990. Biochemical diagnosis of occupational exposure to lead toxicity. Bull Environ Contamin Toxicol 44 268-275. 

Occupational safety healthy administration. Occupational safety and healt standards. Z. Toxic and hazardous substances. 1910-1025 App A. Substance data sheet for occupational exposure to lead. Consulted on March 2012. http //www.osha.gov/pls/oshaweb/owadisp. show document p id= 10031 p table=ST AND ARDS... 

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... 

Lead is an acute and a chronic toxicant. Acute effects are ataxia, headache, vomiting, stupor, hallucination, tremors and convulsions. Chronic symptoms from occupational exposure include weight loss, anemia, kidney damage and memory loss. (Patnaik, P. 1999. A Comprehensive Guide to the Hazardous Properties of Chemical Substarwes, 2nbrain damage has been noted among children. Lead bioaccumulates in bones and teeth. The metal is classified as an environmental priority pollutant by the US EPA. 

Occupational and environmental poisoning with metals, metalloids, and metal compounds is a major health problem. Exposure in the workplace is found in many industries, and exposure in the home and elsewhere in the nonoccupational environment is widespread. The classic metal poisons (arsenic, lead, and mercury) continue to be widely used. (Treatment of their toxicities is discussed in Chapter 57.) Occupational exposure and poisoning due to beryllium, cadmium, manganese, and uranium are relatively new occupational problems, which present new and previously unaddressed problems. 

Mark Cullen is professor of medicine and public health at Yale University School of Medicine. His research interests are in occupational and environmental medicine, including isocyanate exposure in automobile-shop workers, lung cancer in people exposed to asbestos, and lead toxicity in workers. He has published several textbooks, including Clinical Occupational Medicine and Textbook of Clinical Occupational and Environmental Medicine. Dr. Cullen received his MD from Yale University and did his residency in internal medicine. He is a member of the DuPont Epidemiology Review Board, a member of the MacArthur Foundation Network on Socioeconomic Status and Health, and a corporate medical director for the Aluminum Company of America. Dr. Cullen is a member of the Institute of Medicine and served as a member of its Board on Health Sciences. 

Lead has no place in internal medical treatment, although lead acetate has retained a very small place as an astringent. Its toxic effects are known primarily from environmental and occupational exposure and occasionally... 

It should be noted that in the majority of the above mentioned studies, metal-induced renal injury was considered as if exposure occurred to only one metal at a time. In reality it is clear that environmental and occupational exposure may involve several metals at the same time and in varying concentrations [34]. It has been shown that with combined exposure various metals may interact with each other and that one metal may alter the potential toxicity of another in either a beneficial or deleterious way. As an example, whilst arsenic has been shown to worsen cadmium-induced nephrotoxicity, data from experimental studies have shown that selenium may protect against the renal effects induced by cadmium [52]. Other studies have shown that the iron status may alter the toxic effects of aluminium at the level of the bone and the parathyroid gland [53,54], whilst in a recent increased lead accumulation was associated with disturbances in the concentration of a number of essential trace elements [55]. 

The objective of this chapter is to put into perspective some of the current knowledge with respect to trace metals and their health implications. Potential adverse health effects of occupational exposures to trace metals are dis cussed cancer (arsenic, beryllium chromium nickel, and perhaps cadmium) chronic lung disease (beryllium and cadmium) neurologic and reproductive disorders (lead and mercury) and kidney disorders (lead and cadmium). Also discussed are the National Institute for Occupational Safety and Health (NIOSH) recommended standards for occupational exposure to several trace metals, the difficulty of establishing safe levels of exposure (particularly for carcinogens), and problems involved in identifying toxic components of trade name products. Special attention is given to the role of chemists to help protect the public health. 

When used as a diagnostic tool, gallium has produced dermatitis in some patients. Gallium can also lead to gastrointestinal distress. There are not any reported cases of gallium toxicity from occupational exposure. 

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. 

Fly ash from municipal waste and industrial waste incinerators contains polychlorinated dibenzo-p-dioxins (PCDDs), including tetrachlorodibenzo-/j-dioxin (TCDD) and polychlorinated dibenzofurans (PCDFs), which are lipophiles, and heavy metals, including chromium, copper, manganese, vanadium, and lead, which are hydrophilesJ29-31 These chemicals have multiple toxicities and are known to impact the human liver, immune system, respiratory system, thyroid, male reproductive function, and CNS J32 34l Several are human carcinogensJ32 35 Enhanced toxic effects are observed in the mixtures of some of theseJ21,22 36 The mixtures of toxicants present in fly ash are complex and the mechanisms for their action on the human body are largely unknown. It is known that occupational exposure to fly... 

One study demonstrated that parental occupational exposures to chlorinated hydrocarbons are associated with increased risks for leukemia, lymphoma, and urinary tract cancers in offspring. Another study showed associations between maternal exposures to solvents and increased incidences of leukemia. These solvents include 1,1,1-trichloroethane, toluene, and other mononuclear aromatic hydrocarbons, mineral spirits, and alkanes. Childhood brain cancers, the second leading cause of childhood cancer, have been associated with parental occupational exposures to toxic chemicals. Industries for which such associations have been found include 10 ... 

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