Document DM6G1X21LZK33BYLoww9BZeXN

Report to Congress on Workers' Home Contamination Study Conducted Under The Workers' Family Protection Act (29 U.S.C. 671a) U.S. DEPARTMENT OF HEALTH AND HUMAN SERVICES PUBLIC HEALTH SERVICE CENTERS FOR DISEASE CONTROL AND PREVENTION NATIONAL INSTITUTE FOR OCCUPATIONAL SAFETY AND HEALTH CINCINNATI, OHIO 45226 SEPTEMBER 1995 DHHS(NIOSH) Publication No. 95-123 DISCLAIMER Mention of any company or product does not constitute endorsement by the National Institute for Occupational Safety and Health. FOREWORD In 1992, the U.S. Congress passed the Workers' Family Protection Act (Public Law 102-522,29 U.S.C. 671), which requested that the CDC's National Institute for Occupational Safety and Health (NIOSH) conduct a study to "evaluate the potential for, prevalence of, and issues related to the contamination of workers' homes with hazardous chemicals and substances...transported from the workplaces of such workers." With this request. Congress identified a compelling public health issue, bridging health concerns in the workplace and the home. NIOSH found that contamination of workers' homes is a worldwide problem, with incidents reported from 28 countries and from 36 States in the United States. Such incidents have resulted in a wide range of diseases and, in some cases, death among workers' families. This report represents an important step in addressing the concerns outlined in the Act. It puts us on the road to preventing the exposure of families to potentially harmful substances unknowingly brought home from the job. It also serves as a reminder of the importance of occupational safety and health research to CDC's overall mission of promoting health and quality of life by preventing and controlling disease, injury, and disability. David Satcher, M.D., Ph.D. Director, Centers for Disease Control and Prevention 1U PREFACE The legislative directive (Public Law 102-522, Section 209, the Workers' Family Protection Act, [29 U.S.C. 671a]) to conduct this study of contamination of workers' homes by substances carried home on workers' clothing or bodies was enacted on October 26, 1992. However, this is not a new problem. Holt [1923] cited two early studies of lead-workers' families that were published in 1860 and 1896. Oliver [1914] reported on lead poisoning in wives of house painters who washed their husbands' overalls, observations that resulted in a series of laws in Great Britain to protect the workers' families from lead poisoning. Lead poisoning continues to be a problem; this report cites about 65 incidents of lead poisoning among workers' families. Of these, 35 are from the United States, 24 of which were reported in the last 10 years. Lehmann [1905] reported that the mother and child of a worker exposed to chlorinated hydrocarbons developed chloracne (a condition similar to acne caused by certain chlorinated chemicals) ascribed to the worker's contaminated clothing. Lehmann also wrote of a laundress who developed chloracne as a result of washing the contaminated clothing of workers. Thirty years after Lehmann's report was published in Germany, a similar case was reported by Fulton and Matthews [1936] from the Pennsylvania Department of Labor and Industry. In this case a child's father who was exposed to hexachloronaphthalene and chlorodiphenyl wore his soiled clothing home from work. Additional cases of workers' homes being contaminated with chlorinated hydrocarbons have been reported in the last 10 years. Prior to 1960, beryllium, toxaphene. mercury vapors, and diethylstilbestrol were also identified as hazards to the families of workers. In the last 10 years, 10 additional chemical substances have been identified in incidents of workers' home contamination, as well as allergens, radioactive materials, and infectious agents. This report to Congress and the Workers' Family Protection Task Force summarizes the incidents of home contamination this study has discovered, including the health consequences, the sources, and the levels of contamination. The report contains information on the effectiveness of preventive measures and of decontamination procedures that have been used or studied. The report summarizes the relevant laws and regulations and responses of Federal and State agencies and industry to incidents of workers' home contamination. The report should be useful not only to Congress and the Workers' Family Protection Task Force in deciding future actions, but also to all who have responsibilities and concern for protecting workers and their families from preventable illnesses. Linda Kosenstock, m.d., M.P.H. Director, National Institute for Occupational Safety and Health v EXECUTIVE SUMMARY The Workers' Family Protection Act of 1992 (Public Law 102-522, 29 U.S.C. 671a) directed the National Institute for Occupational Safety and Health (NIOSH) to conduct a study of contamination of workers* homes with hazardous chemicals and substances (including infectious agents) transported from the workplace. NIOSH found that contamination of workers' homes is a worldwide problem; incidents have been reported from 28 countries and from 36 States in the United States. Such incidents have resulted in a wide range of health effects and death among workers' families exposed to toxic substances and infectious agents. About half of the reports of health effects have appeared in the last 10 years, revealing new sources of contamination. In completing the study, NIOSH solicited information from Federal and State health, labor, and environmental agencies, groups with special circumstances such as firefighters, and the public. NIOSH then reviewed and compiled the information received along with information in published reports on contamination of workers' homes by substances brought home from the workplace. The report includes a survey of reported health effects, information on sources and levels of contamination, preventive measures, decontamination procedures, a review of Federal and State laws, and responses of agencies and industry to incidents involving contamination of workers' homes. This report is being considered by the Workers' Family Protection Task Force, which is charged under the Workers' Family Protection Act with evaluating the need for additional research. Health Effects of Workers* Home Contamination Workers can inadvertently carry hazardous materials home from work on their clothes, skin, hair, tools, and in their vehicles. As a result, families of these workers have been exposed to hazardous substances and have developed various health effects. Health effects have also occurred when the home and the workplace are not distinct-such as on farms or in homes that involve cottage industries. For some contaminants, there are other potential sources of home contamination such as air and water pollution and deteriorating lead paint in the home. Only a few of the studies found in the literature used epidemiologic methods to estimate the relative risks of health effects from the contaminant transported home by the worker independent of health risks due to other sources of the contaminant in the home. little is known of the full range of health effects or the extent to which they occur as a result of workers' home contamination. There are no information systems to enable tracking of illnesses and health conditions resulting from these circumstances. Many of the health effects among workers' family members described below were recognized because of their uniqueness their clear relationship to workplace contaminants, or their serious nature. vu Chronic beryllium disease This potentially fatal lung disease has occurred in families of workers exposed to beryllium in the nuclear and aviation industries and workplaces involved in the production of beiyllium and fluorescent lights and gyroscopes. Asbestosis and mesothelioma Fatal lung diseases have occurred among family members of workers engaged in the manufacture of many products containing asbestos, including thermal insulation materials, asbestos cement, automobile mufflers, shingles, textiles, gas masks, floor tiles, boilers, ovens, and brakeshoes and other friction products for automobiles. Families have also been exposed to asbestos when workers were engaged in mining, shipbuilding, insulating (e.g., pipe laggers and railway workers), maintenance and repair of boilers and vehicles, and asbestos removal operations. Lead poisoning, neurological effects, and mental retardation These health effects have occurred in children of workers engaged in mining, smelting, construction, manufacturing (pottery, ceramics, stained glass, ceramic tiles, electrical components, bullets, and lead batteries), repair and reclamation of lead batteries, repair of radiators, recovery of gold and silver, work on firing ranges, and welding, painting, and splicing of cables. Deaths and neurological effects from pesticides Farm families and families of other workers exposed to pesticides have suffered these serious effects. Chemical burns from caustic substances Chemical bums of the mouth and esophagus and fatalities from ingesting caustic substances have occurred in farm families when hazardous substances were improperly used and stored on farms. Chloracne and other effects from chlorinated hydrocarbons Family members have been exposed when these substances were transported home on clothing of workers manufacturing or using these compounds in the production of insulated wire, plastic products, ion exchange resins, and textiles. Family members have been similarly exposed when workers' clothes became contaminated during marine electrical work, transformer maintenance, municipal sewage treatment, rail transportation, wood treatment, and application of herbicides. Neurological effects from mercury Family members have developed various neurological effects as a result of being exposed to mercury carried home on clothing of workers engaged in mining, thermometer manufacture, and cottage-industry gold extraction.  Abnormal development from estrogenic substances Enlarged breasts have occurred in boys and girls and premature menstruation has occurred in girls from estrogenic substances brought home on contaminated clothing of pharmaceutical and farm workers. Asthmatic and allergic reactions from dusts Farm families and others have suffered asthmatic and other allergic effects from animal allergens, mushrooms, grain dust, and platinum salts. Liver angiosarcoma from arsenic Families of workers engaged in mining, smelting, and wood treatment have been exposed to arsenic from contaminated skin and clothing; one child developed liver angiosarcoma. Dermatitis from fibrous glass Family members have developed dermatitis when their clothing was contaminated with fibrous glass during laundering of insulation workers' clothing. Status epilepticus from chemical exposure A child experienced epileptic seizures following ingestion of an explosive compound brought home on the clothing of a worker engaged in the manufacture of explosives. Diseases from infectious agents Family members have contracted infectious diseases such as scabies and Q fever from agents brought borne on contaminated clothing and skin of workers engaged in agriculture, hospital, and laboratory work. As intended by Congress, infectious agents are included as hazardous substances to the extent that pathogens can be transported on a worker's person or clothing. Measures for Preventing Home Contamination Preventive measures that were found to be effective when used in the workplace include: Reducing exposures in the workplace; Changing clothes before going home and leaving the soiled clothing at work to be laundered by the employer, Storing street clothes in separate areas of the workplace to prevent their contamination; Showering before leaving work; and Prohibiting removal of toxic substances or contaminated items from the workplace. Preventive measures that have been used successfully at home include: Separating work areas of cottage industries from living areas; Properly storing and disposing of toxic substances on farms and in cottage industries; ix  Preventing family members from visiting the workplace; Laundering contaminated clothing separately from family laundry when it is necessary to launder contaminated clothing at home; and Informing workers of the risk to family members and of preventive measures. Other preventive measures that need to be used include: Educating physicians and other health professionals to inquire about potential workrelated causes of disease; Developing surveillance programs to track health effects that could be related to home contamination; and Educating children, parents, and teachers about the effects of toxic substances. Procedures for Decontaminating Homes and Clothing Decontamination procedures include air showers, laundering, airing, vacuuming and other methods of surface cleaning, and destruction and disposal of contaminated items. These procedures appear to have widely varying effectiveness, depending on the specific methods employed, the contaminants, and the surfaces. In general, hard surfaces can be far more easily decontaminated than clothes, carpets, and soft furniture. In most cases effective decontamination requires relatively intensive methods. Normal house cleaning and laundry practices appear to be inadequate for decontaminating workers' clothes and homes. Lead, asbestos, pesticides, and beryllium contamination can be especially persistent. In some instances even intensive decontamination procedures may be ineffective. Another serious concern is that decontamination methods can increase the hazard to the person performing the operation and to others in the household. Home laundering of contaminated clothing exposes the launderer. Vacuuming of floors contaminated with mercury can substantially increase air concentrations, and vacuuming of carpets contaminated with lead can increase lead concentrations on the carpet surface. The difficulty of decontaminating work clothing, the prominence of clothing as a source of home contamination, and the potential exposure of the launderer are problems that can be avoided through the use of disposable work clothing. The use, availability, and cost of this alternative need to be assessed. Federal and State Laws Seven statutes provide Federal agencies with some mechanisms for responding to or preventing workers' home contamination. Twenty rules or standards in the Code of Federal Regulations (CFR) address workers' home contamination or have elements that serve to protect workers' families. x Under the Occupational Safety and Health Act of 1970 (Public Law 91-596), NIOSH research assessing the health of workers has also addressed the exposure of their families to workplace contaminants, resulting in recommendations to prevent home contamination. The Occupational Safety and Health Administration (OSHA) regulations and actions intended to protect workers also help assure that families are protected. In addition, OSHA can promulgate standards to protect workers' family members when workers are required to live in housing provided by the employer as a condition of employment Under the Federal Mine Safety and Health Act of 1977 (Public Law 95 164), the Mine Safety and Health Administration (MSHA) has limited regulatory authority to address issues of workers' home contamination. The U.S. Environmental Protection Agency (EPA) has broad authority under the Toxic Substances Control Act (Public Law 94-469) to regulate chemicals and to obtain information about the adverse effects of chemicals. In addition, EPA has specific authority and responsibility regarding the use of asbestos and lead. Under the Federal Insecticide, Fungicide, and Rodenticide Act (Public Law 92-516), EPA also regulates the use and disposal of pesticides (which also helps to protect workers' families). EPA and the Agency for Toxic Substances and Disease Registry (ATSDR) are authorized under the Superfimd Amendments and Reauthorization Act of 1986 (Public Law 99-499) to address hazardous waste and releases of hazardous substances that may relate to identifying contamination of workers' homes and assuring decontamination. Thirty States and Puerto Rico responded to the requests from NIOSH for information about State laws. Most indicated that there were no laws specific to workers' home contamination or protection of workers' family members. Some States identified laws requiring the reporting of cases of elevated blood lead levels and pesticide poisonings to a State agency; other States identified laws related to work at hazardous waste sites and emergency responses to releases of hazardous substances. An examination of occupational safety and health regulations of States with OSHA-approved occupational safety and health programs revealed none more stringent than Federal OSHA regulations - with respect to the protection of workers' families. However, extension of occupational safety and health regulations to State and local government employees in these States also helps protect the families of public employees* in these States. Responses to Incidents of Workers' Home Contamination Several Federal agencies have responded to incidents of workers' home contamination, often working together with State or local government agencies. These responses have resulted in identification of workers' home contamination, decontamination of workers' homes, and recommendations for instituting workplace changes that would prevent further contamination. NIOSH has conducted approximately 40 health hazard evaluations that address potential home contamination. In several cases, Federal agencies have referred incidents to State or local health departments for follow-up actions. XI State agencies have investigated incidents of workers' home contamination, made referrals to Federal agencies for follow-up actions, and recommended workplace improvements to prevent further contamination of workers' homes. Responses to incidents of workers' home contamination include educational materials such as those of the Lead Industries Association, Inc. on preventing workers' home contamination as well as responses of various employers to specific incidents of home contamination. limitations of the Report The health information available for the report, which indudes inddents of illness and home contamination obtained from public agenties and published literature, does not provide a basis for estimating the prevalence of this public health problem. The Workers' Family Protection Act requires NIOSH to evaluate relevant information about indoor air quality as it relates to workers' home contamination and to study the sperial circumstances of firefighters as they relate to contamination of their homes. The only report found on indoor air quality applicable to workers' family protection involved tetracbloroethylene exposures in living quarters located in the same building as dry-cleaning establishments. Indoor air quality studies would be useful to protect family members in cottage industries. Inddents of contamination of firefighters' homes were not identified. However, NIOSH has conducted several studies of contamination and decontamination of protective clothing used by firefighters. These studies are reviewed in this report and NIOSH will continue to pursue the issues related to potential contamination of firefighters' homes. Other limitations of the report indude: Little research has documented the frequency and distribution of health effects among the families of workers in various industries and occupations. NIOSH is undertaking one study addressing lead exposure among families of bridge repair workers. Lead and pestiddes are the only contaminants for which monitoring or reporting programs help to identify and prevent cases of poisoning from workers' home contamination. Despite various case reports, the prevalence of health effects from workers' home contamination is not known because there are no surveillance systems in place for tracking or monitoring such health conditions. Many diseases have long latency periods between exposure and manifestation of the disease, making identification and intervention difficult. Xll  The workplace origin of many common diseases that occur in workers' families (such as asthma, dermatitis, and infectious diseases) is probably unrecognized because physicians and other health professionals fail to inquire about the occupation of family members and to consider whether these diseases are work-related. The literature reviewed in this report contained only nominal information about contamination levels in workers' homes. Most measurements were of surface dust, for which there are no guidelines for acceptable levels of contamination. Recommendations for Research and Education The prevalence of health effects of contaminants transported from the workplace should be determined. One possible approach would be to conduct surveys among occupational and environmental medicine health care providers and clinics. The employment practices and controls that work best in preventing the transport of contaminants from the workplace to the home should be identified. Educational programs to prevent home contamination should be developed for employers, workers, children, teachers, and parents, physicians, and other health professionals. The special needs and problems of individuals who work in home or cottage industries need to be identified. Conclusions Workers' home contamination may pose a serious public health problem. Health effects and deaths from contaminants brought home from the workplace have been reported in 28 countries and 36 States. The extent to which these health effects occur is not known because there are no information systems to track them, and physicians do not always recognize the occupational contribution to various common diseases. About half of the reports of health effects from home contamination are less than 10 years old. The literature on the health effects involved approximately 30 different substances or agents. The potential exists for many of the thousands of other chemicals used in commerce to be transported to workers' homes or to be used in home-centered businesses. Health effects and deaths from contaminants brought home from the workplace are preventable using known effective measures. Educational programs are needed to promote their use. xiii  Normal bouse cleaning and laundry practices are often inadequate for decontaminating workers' homes and clothing and can increase the hazard to the person performing the tasks and others in the household. Only two Federal laws have elements that directly address workers' home contaminatioa However, other laws provide agencies with certain mechanisms for responding to, or preventing workers' home contamination. Operating under existing laws OSHA, MSHA, DOE, ATSDR, EPA and CDC, including NIOSH and the National Center for Environmental Health have responded to incidents of workers' home contamination, made recommendations to prevent such incidents, and conducted relevant research. XIV TABLE OF CONTENTS FOREWORD .......................................................................................................................... iii PREFACE......................................................................................................................................v EXECUTIVE SUMMARY................................................................................................ vii Health Effects of Workers' Home Contamination....................................... vii Measures for Preventing Home Contamination............................................................. ix Procedures for Decontaminating Homes and Clothing.......................................................x Federal and State Laws ..........................................................................................................x Responses to Incidents of Workers' Home Contamination.............................................. xi Limitations of the Report................................................................................................ xii Recommendations for Research and Education...............................................................xiii Conclusions ........................................................................................................................... xiii INTRODUCTION............................................................................................. xxiii CHAPTER 1. HEALTH EFFECTS OF WORKERS' HOME CONTAMINATION . 1 CHAPTER SUMMARY ................................................................................................... 1 BERYLLIUM ..................................................................................................................... 3 Overview........................................................................................................................ 3 Background................................................................................................................... 3 Review of Studies ....................................................................................................... 4 ASBESTOS.......................................................................................................................... 6 Overview........................................................................................................................ 6 Background................................................................................................................... 6 Review of Studies ....................................................................................................... 7 Cohort Studies.......................................................................................................... 8 Community-Based Cohort Studies.......................................................................... 9 Case-Control Studies.............................................................................................. 9 Case Reports.......................................................................................................... 10 Case-Series ............................................................................................................ 11 LEAD................................................................................................................................. 11 Overview..................................................................................................................... 11 Background................................................................................................................. 12 Review of Studies of Blood Lead Levels ............................................................. 13 Cohort Studies....................................................................................................... 14 Community Studies................................................................................................. 15 Case Reports and Case Series ........................................................................... 15 Review of Studies of Other Health Effects........................................................... 15 CAUSTTC FARM PRODUCTS..................................................................................... 16 Overview..................................................................................................................... 16 xv TABLE OF CONTENTS Background................................................................................................................. Review of Studies ..................................................................................................... PESTICIDES..................................................................................................................... Overview..................................................................................................................... Background................................................................................................................. Review of Studies ..................................................................................................... CHLORINATED HYDROCARBONS.................... Overview..................................................................................................................... Background................................................................................................................. Review of Studies .......................................................................... MERCURY........................................................................................................................ Overview..................................................................................................................... Background................................................................................................................. Review of Studies ..................................................................................................... ESTROGENIC SUBSTANCES.................................................................................... Overview..................................................................................................................... Background................................................................................................................ Review of Studies ..................................................................................................... ASTHMATOGENS/ALLERGENS.............................................................................. ARSENIC.......................................................................................................................... CADMIUM....................................................................................................................... FIBROUS GLASS............................................................................................................ OTHER SUBSTANCES ................................................................................................ INFECTIOUS AGENTS ................................................................................................ Overview..................................................................................................................... Background................................................................................................................ Review of Studies ..................................................................................................... RADIOACTIVE SUBSTANCES.................................................................................. 16 16 17 17 18 18 20 20 20 20 22 22 22 22 24 24 24 24 25 26 26 27 27 27 27 28 32 33 CHAPTER 2. SOURCES OF WORKERS' HOME CONTAMINATION................. CHAPTER SUMMARY ................................................................................................ CONTAMINATED CLOTHING.................................................................................. Overview..................................................................................................................... Beryllium................................................................................................................. Asbestos ................................................................................................................. Lead........................................................................................................................ Overview........................................................................................ Reports of clothing and home contamination........................................... Supporting studies......................................................................................... Pesticides................................................................................................................. Chlorinated Hydrocarbons.................................................................................. Mercury................................................................................................................... 34 34 35 35 35 36 37 37 37 38 39 41 41 xvi TABLE OP CONTENTS Estrogens.............................................................................................................. Other Substances................................................................................................ Infectious Agents................................................................................................ Radioactive Substances ..................................................................................... THE WORKER'S BODY ............................................................................................ TOOLS AND EQUIPMENT....................................................................................... TAKING ITEMS HOME FROM WORK ................................................................ Beryllium.................................................................................................................. Asbestos .................................................................................................................. Lead......................................................................................................................... Pesticides ................................................................................................................ Estrogens ................................................................................................................ Radioactive Substances ......................................................................................... COTTAGE INDUSTRIES............................................................................................ Asbestos .................................................................................................................. Lead......................................................................................................................... Pesticides ................................................................................................................ Mercury..................................................................................................................... FARMS........................................................................................................................... FAMILY VISITS TO WORKPLACE......................................................................... 42 43 43 43 43 44 44 44 45 45 45 45 45 45 46 46 47 47 47 48 CHAPTER 3. LEVELS OF CONTAMINATION IN HOMES AND CARS............ CHAPTER SUMMARY .............................................................................................. ASBESTOS..................................................................................................................... LEAD.............................................................................................................................. Concentrations of Lead in Dust............................................................................ Lead Loading ......................................................................................................... MERCURY..................................................................................................................... CHLORINATED HYDROCARBONS....................................................................... PESTICIDES.................................................................................................................. ARSENIC....................................................................................................................... INFECTIOUS AGENTS .............................................................................................. 49 49 50 50 50 51 52 52 52 53 53 CHAPTER 4. PREVENTIVE MEASURES.................................................................. CHAPTER SUMMARY .............................................................................................. BERYLLIUM................................................................................................................ ASBESTOS..................................................................................................................... LEAD.............................................................................................................................. CAUSTIC FARM PRODUCTS.................................................................................. PESTICIDES.................................................................................................................. HORMONES ................................................................................................................ ASTHMATOGENS/ALLERGENS ............................................................................ 54 54 54 55 55 57 57 59 60 xvu TABLE OF CONTENTS CHAPTER 5. DECONTAMINATION PROCEDURES.............................................. CHAPTER SUMMARY ............................................................................................. DECONTAMINATION GUIDELINES.................................................................... REVIEW OF DECONTAMINATION PROCEDURES......................................... BERYLLIUM............................................................................................................... ASBESTOS................................................................................................................... LEAD............................................................................................................................. PESTICIDES................................................................................................................. CHLORINATED HYDROCARBONS....................................................................... MERCURY.................................................................................................................... OTHER SUBSTANCES ............................................................................................. INFECTIOUS AGENTS ............................................................................................. 61 61 61 62 62 62 63 64 68 69 70 70 CHAPTER 6. REVIEW OF EXISTING FEDERAL AND STATES LAWS......... CHAPTER SUMMARY ............................................................................................. FEDERAL LAWS........................................................................................................ STATE LAWS............................................................................................................... BACKGROUND........................................................................................................... REVIEW OF RELEVANT FEDERAL STATUTES AND RULES..................... Occupational Safety and Health Act of 1970 (OSH Act).................................. OSHA................................................................................................................. NIOSH................................................................................................................ Federal Mine Safety and Health Act of 1977 (Mine Act) ................................ Toxic Substances Control Act (TSCA)................................................................ Asbestos Hazard Emergency Response Act of 1986 ......................................... Residential Lead-Based Paint Hazard Reduction Act of 1992 ......................... Federal Insecticide, Fungicide, and Rodenticide Act (FIFRA) ....................... Comprehensive Environmental Response, Compensation, and Liability Act (CERCLA) and Superfund Amendments and Reauthorization Act (SARA) REVIEW OF STATE LAWS...................................................................................... 72 72 72 73 73 75 75 75 77 77 78 79 79 79 81 82 CHAPTER 7. RESPONSES TO INCIDENTS OF HOME CONTAMINATION ... CHAPTER SUMMARY ............................................................................................. RESPONSES OF FEDERAL AGENCIES................................................................ OVERVIEW................................................................................................................. Centers for Disease Control and Prevention (CDQ......................................... National Center for Environmental Health (NCEH)..................................... National Institute for Occupational Safety and Health (NIOSH)................ Asbestos...................................................................................................... Lead............................................................................................................. Chlorinated Hydrocarbons......................................................................... Mercury ...................................................................................................... Estrogenic Substances................................................................................ 84 84 84 84 85 85 86 86 87 87 87 87 xvin table of contents Agency for Toxic Substances and Disease Registry (ATSDR).......................... Occupational Safety and Health Administration (OSHA) ................................ Mine Safety and Health Administration (MSHA).............................................. Environmental Protection Agency (EPA)....................................... Department of Energy (DOE).............................................................................. Nuclear Regulatory Commission (NRC).............................................................. RESPONSES OF STATE AGENCIES....................................................................... Lead............................................................................. Pesticides ................................................................................................................. Other ....................................................................................................................... RESPONSES OF INDUSTRY..................................................................................... 88 88 89 89 89 91 93 93 96 96 97 CHAPTER 8 - RECOMMENDATIONS AND CONCLUSIONS ................................... 98 Recommendations for Research and Education...............................................................98 Conclusions .......................................................................................................................... 98 REFERENCES................................................................................................................... 99 xix [1957] reported on five persons with beryllium disease who had exposure to clothing of beryllium extraction workers. Other authors [DeNardi et al. 1949; Sussman et al. 1959; Eisenbud and Lisson 1983] discuss varying numbers of contact (household) cases. The cases discussed by these authors are likely included in the Beryllium Case Registry, but it is difficult to be certain of this because detailed descriptions are not always given. According to the literature review, there were no more contact (household) cases added to the registry after Hardy et al. [1967] until the article by Newman and Kreiss [1992] who reported on a 56-year-old woman with chronic beryllium disease who had first been diagnosed with sarcoidosis. When it was determined that her husband was a beryllium worker, she was evaluated for beryllium disease. The clinical picture was compatible with beryllium disease and her blood test showed beryllium sensitization. Because of the long period of time between the prior contact cases and this case, a review of her exposures to beryllium is useful. She was a non-smoker who had always lived in Ohio. She was self-employed and had sold cosmetics, done babysitting, brought up her children, and from 1973 until the time of the article, had done stockroom work for a retailer. Her husband had worked from 1959 to the current time at a beryllium production plant, with daily exposure to beryllium. When working directly with beryllium, he always changed clothing after work, showered before leaving for home, and did not bring his work clothing home. The family had always lived at least 28 miles from his work. She sought medical attention for this illness in November 1988. Her exposures consisted of the following: She took a tour of the plant in the 1960's; She took another tour in the 1970's at a time when it was not operating; During some months in 1976, her husband was an advisor to a new ceramics plant, where be did not do hands-on work and wore street clothes, which his wife cleaned on several occasions. Thus although beryllium was used at the plant, clothes worn to work were not left at work; A hydrogen furnace containing beryllium oxide exploded in her husband's face in February 1979. He was sent to the emergency room in his contaminated work clothes. When he was discharged from the emergency room, she was given the contaminated clothes which she put in a plastic bag at home before returning them to the plant guardhouse. Over the next several months, she scrubbed her husband's face several times daily with a motorized rotating brush to remove embedded metallic debris; and The husband injured his ankle while at work in September 1987. When she picked him up at the hospital, he was still wearing work clothes. He rode home in her car and she placed the dusty clothes in a plastic bag. 5 This case illustrates the need for vigilant application of industrial hygiene controls for beryllium even when exposures do not seem high or consistent Moreover, it is possible that household and community cases of beryllium disease may still he occurring but are unrecognized or misdiagnosed as in this case. ASBESTOS Overview Based on the studies reviewed in this section, families of asbestos-exposed workers have been at increased risk of pleural, pericardial, or peritoneal mesothelioma, lung cancer, cancer of the gastrointestinal tract, and non-malignant pleural and parenchymal abnormalities as well as asbestosis. Four cohort studies (Table 2), one community study (Table 3), seven case-control studies CTable 4), numerous case reports . (Table 5) and case series (Table 6) provide evidence of these adverse effects in family members of asbestos workers. ^ The occupations associated with asbestos-related disease in family members are those where workers were exposed to asbestos dust during: construction and renovation; prospecting and mining; manufacturing textiles, tiles, boilers, and ovens; shipbuilding and associated trades; certain railroad shop trades; welding; insulation; use and manufacture of asbestos products such as cords, seals, and plates; and renovation and demolition projects within the construction industry. Although many past uses of asbestos have been abandoned, and asbestos uses and occupational exposures are now subjected to regulation, potential exposures of family members in the United States may still exist, especially in the construction industry [Sullivan et al. 1995]. Background Asbestos is a generic term for a number of silicate minerals with a fibrous crystalline structure. The asbestiform varieties of silicate minerals can be found in both the amphibole and serpentine mineral groups, in veins or small veinlets within rock containing or composed of the common (non-asbestiform) variety of the same mineral. The major asbestiform varieties of minerals used commercially are chiysotile, tremolite-actinolite asbestos, cummingtonite-grunerite asbestos, anthophyllite asbestos, and crotidolite. Asbestos is marketed by its mineral name (e.g., anthophyllite asbestos), its variety name (e.g., chrysotile, crocidolite), or its trade name (e.g., Amosite). Mesothelioma is a tumor arising from the pleural, pericardial, and peritoneal membranes. When it occurs in asbestos workers' household contacts, it is a sentinel event for exposure to asbestos from home contamination [Gardner and Saracd 1989]. Lung cancer is a malignant tumor of the lung. Cancer of the gastrointestinal tract is a malignant tumor of any part of the gastrointestinal tract including the mouth, pharynx, esophagus, stomach, small intestine, pancreas, colon, rectum, and anus. Asbestosis is a fibrotic disease of the lungs caused by 6 asbestos fibers which results in reduced lung volumes and difficulty in breathing. Pleural and hyaline plaques are localized thickenings which may be evident on radiographs 20 or more years after exposure. Pleural and hyaline plaques generally occur without symptoms but do provide a clinical marker of asbestos exposure. Mesothelioma has occurred following short term asbestos exposures of only a few weeks, and can result from very low levels of exposure. There may be a latency period of 40 years or longer between exposure and clinical disease. Symptoms include chest pain, shortness of breath, and weight loss. Analysis of tissue obtained by biopsy (or at autopsy) is required for a definitive diagnosis (Dement et al. 1986]. Treatment is ineffective, with rapid disease progression and dead [Lilis 1986], . Lung cancer may be associated with a range of symptoms including cough, shortness of breath, bloody sputum, and weight loss. Definitive diagnosis is muu. by tissue biopsy. Metastasis is common, and may present as bone pain or fracture, seizure, or various other syndromes. Progression of lung cancer is generally rapid, and treatments (including surgery, chemotherapy, and radiation) are unlikely to result in long term survival [Hodous and Melius 1986]. Although increased risk of lung cancer among household contacts of asbestos workers has been observed, the high prevalence of cigarette smoking among lung cancer cases frequently makes it difficult to detect cases which may be caused by exposure to asbestos resulting from workers' inadvertent contamination of the home. Review of Studies Information on exposure of family members has been elicited by questioning patients or relatives about the practice of bringing work clothes home and laundering the asbestos contaminated clothing at home. Other identified sources of exposure of workers' family members to asbestos include taking contaminate items home from work and using asbestos in cottage industries [Magee et al. 1986; Bittersohl and Ose 1971], Additional evidence that exposures occurred in the homes of asbestos workers is the finding of asbestos in lungs of asbestos workers' family members who had no known exposures, other than contact with an exposed worker [Whitwell et al. 1977; Ashcroft and Heppleston 1970; Huncharek et al. 1989; Gibbs et al. 1989, 1990; Giarelli et al. 1992]. Most cases of asbestos disease among workers' family members occurred in households where information indicated that asbestos-contaminated work clothing was brought into the home and women were exposed during home laundering of the contaminated work clothing [Ashcroft and Heppleston 1970; Dalquen et al. 1970; Edge and Choudhury 1978; Lander and Viskum 1985; Konetzke et al. 1990]. Children were exposed by playing in areas where asbestos-contaminated shoes and work clothes were located, or where products containing asbestos were used or stored. It is of interest to note that male children of asbestos workers appear to 7 CHAPTER 2. SOURCES OF WORKERS' HOME CONTAMINATION CHAPTER SUMMARY Sources of contamination of workers homes and poisonings of workers' family members reviewed in this chapter include: work clothing; the worker's body; tools and equipment; taking items home from work (such as scrap material); cottage industries (where work is done in or adjacent to the home); farms; and visiting a family member's workplace. Clothing contamination was documented in 18 reports: 1 on beryllium; 7 on lead; 7 on pesticides; and 1 each on PCB's, an estrogenic substance (zeranol), and 3,4benzo(a)pyrene. For lead, measurements of both clothing and home contamination were included in some studies. However, these were inadequate for establishing a quantitative relationship between the two. Other evidence of clothing as a source of home contamination includes: high levels of contamination in areas of homes where soiled clothing is stored and laundered (lead, mercury); contamination of washing machines (mercury) or dryers (3,3'*dichlorbenzidine, MOCA); and poisoning of launderers (beryllium, asbestos, lead, kepone). The workers' body has been considered as a source of home contamination, and showering before leaving work has often been recommended as a preventive measure. However, reports have only documented contamination of workers' hands. Hand tools and other equipment have been found to contribute to home and vehicle contamination by mercury and pesticides. The potential for contamination of homes by tools was also demonstrated for PCB's and radioactive substances. Items taken home from work (beryllium-ore bags, cotton shipping-bags for asbestos, cloths from discarded filters, metal drums, contaminated milk, and radioactive scrap lumber) have resulted in serious, and sometimes fatal, poisonings of workers' family members. Cottage industries, where work is undertaken in the same building or on the property where the family resides have been recognized as a hazard to family members since at least 1914. Cottage industries are the subject of 22 reports of home contamination or family poisonings from asbestos, lead, parathion, and mercury which are reviewed in this chapter. The levels of contamination were often extremely high and the poisonings were severe. Farms are similar to cottage industries in that families live on the property where work is performed. Three types of products used on farms: pesticides; caustic substances; and estrogenic substances have resulted in several cases of poisoning of family members. - 34 Visiting the workplace of a family member has been shown to be a hazard for families of dry cleaners and veterinarians. CONTAMINATED CLOTHING Overview This section reviews reports that provide evidence for clothing worn, or otherwise taken home from work, as a source of home contamination. The reports are summarized in Table 15. In the health effects studies reviewed in Chapter 1, home contamination and family exposures were often attributed to contaminated clothing brought home from the workplace. This attribution was based on: information elicited by questioning household members; descriptions of workplaces and work practices; and the practice of wearing and laundering work clothes at home. Clothing contamination was documented in 18 reports reviewed below. 1 on beryllium; 7 on lead; 7 on pesticides; 1 on chlorinated hydrocarbons (PCBs); 1 on an estrogenic substance (zeranol); and 1 on 3,4-benzo(a)pyrene. Only for lead were measurements of both clothing contamination and home contamination included in the same studies; these few studies are inadequate for establishing any quantitative relationship between clothing contamination and home contamination. Other evidence of clothing as a source of home contamination includes: the findings discussed below of high levels of contamination in laundry areas of workers' homes and in areas where contaminated clothing is stored (lead, mercury); contamination of washing machines (mercury) or dryers (3, 3'dichlorbenzidine, MOCA); and poisoning of home launderers (beryllium, asbestos, lead, kepone). Estimates of exposure levels that could have occurred during home laundering of beryllium and asbestos suggest that such exposures could have exceeded OSHA occupational exposure limits for these substances. Beryllium There were no reports of measurements of home contamination by beryllium, although the case histories and epidemiology studies generally assumed that cases of berylliosis in workers' family members were due to laundering contaminated clothing. In support of this assumption, the following studies on clothing contamination indicate that substantial amounts of beryllium dust could have been brought into the workers' homes by contaminated clothing. Fabrics experimentally exposed at a beryllium production worksite contained beryllium up to 2.8 mg/m1 [Bohne and Cohen 1985]. In a subsequent study Cohen and Positano [1986], found that work shirts contained from 12 to 37 mg/m1 of beryllium. It is likely that inhalation exposures of workers' family members occurred during laundering of the contaminated clothing, since resuspended beryllium dust concentrations in air from unwashed shirts at up to 0.64 ftg/m1 were found. In an earlier laboratory study, Eisenbud et al. [1949] found beryllium concentrations in air at 125-1,200 fig/m* when soiled clothes 35 were shaken and estimated an inhalation dose of 17 /ig during a single home laundiy. The OSHA permissible exposure limit (PEL) for beryllium is 2 jig/m3 as an 8-hr. time-weighted average (TWA) with permissible excursions up to 25 Mg/m3 for up to 30 minutes (29 CFR11910.1000). Asbestos Several studies of asbestos workers' families inferred that asbestos-related diseases were due to home contamination emanating from clothes contaminated at work, especially due to laundering the clothes [Anderson et aL 1979a,b; Bianchi et al. 1987; Giarelli et al. 1992; Gibbs et ah 1990; Huncharek et aL 1989]. However, no studies evaluated the relationships between home contamination by asbestos, contamination of clothing brought home from work, and exposures during home laundering. The few studies reported and reviewed in this section indicate that dothing probably was a source of home contamination by asbestos and support the hypothesis that home laundering of asbestos contaminated dothing could be especially hazardous. One study reported measurements of asbestos contamination in workers' homes; however no measurements of dothing as a source of the contamination were made [Nicholson et al. 1980]. Two studies of workplace clothing contamination by asbestos have been reported [Seixas and Ordin 1986; Driscoll and Elliott 1990]. Chiysotile asbestos was found in all dothing vacuumed as employees left work at a brake shoe manufacturing facility, but neither report provided quantitative data on asbestos recovered from the workers' dothing. No studies of exposure during home laundering were found. However, a study on laundering clothing contaminated by an asbestos removal operation produced an average of 0.4 fibers/cm3 while picking up dothing and loading the washer. A maximum of 12 fibers/cm3 was found during the total laundiy operation [Sawyer 1977]. Although the study was not conducted in a home laundry and measurements of the level of dothing contamination that generated these concentrations were not made, the study is consistent with the hypothesis that home laundering of asbestos-contaminated dothing is hazardous. Another important aspect of laundering asbestos contaminated dothing is that the fibers can transfer to uncontaminated dothing washed with the contaminated clothing, as was found by NIOSH [1971] in a study of dry cleaning a coat made with 8% asbestos fiber. </ ^ ^Code of Federal Regulations. See CFR in references. 36 Asbestos Asbestos-contaminated cotton cloth bags that had been used to transport molded asbestos insulation were taken home by a worker and used as diapers (Li et al. 1989]; three family members died of mesothelioma at an early age. It should be noted that dirty clothes were also brought home. Lead Lead-contaminated cloths from discarded pollution control filters at a lead smelter were taken home by workers for use at home [Carvalho et aL 1984], The children of these lead workers had a mean BLL of 67.5 /ig/dL. In another case, discarded lead battery casings were taken home for fuel by a worker engaged in recovering lead from used batteries [Dolcourt et al. 1981]. The battery casings were burned in the family's wood-burning stove. House dust contained up to 43,281 ppm of lead; one child had a BIX of 220 /xg/100 mL and developed encephalopathy with seizures. Osorio [1994] reported that when lead contaminated telephone poles were taken home for fire wood by a worker, the soil in the yard of the worker's home where the poles were located contained lead at 1,500-1,600 Aig/dX Pesticides Toxaphene-contaminated metal brought home from a processing plant resulted in the death of 2-year-old boy [McGee et aL 1952]. The metal, which consisted of flattened strips made from drums that had contained toxaphene, was used to cover the walls of a tool shed on the day the child, who played in the area, was poisoned. In another case, a loaded company truck was parked in an employees driveway overnight [Barnett 1994]. Part of the load was chloropicrin which leaked from the vehicle, poisoning the next-door neighbors. Estrogens Diethylstilbestrol poisoning of family members was considered by Pacynsld et aL [1971] to be due in part to women bringing home contaminated factory-supplied milk which was consumed by the children. Radioactive Substances Radioactive waste lumber was used to construct a garage at home by a worker engaged in the manufacture of catalysts containing depleted uranium. About 20 years later the garage was found to be contaminated in excess of NRC release criteria [Brockman 1993]. COTTAGE INDUSTRIES Cottage industries, those where work is undertaken in the same building or on the property where the family resides have been recognized as a hazard since at least 1914 [Oliver 1914], Poisonings by asbestos, lead, parathion, and mercury have occurred in cottage industries. 45 Asbestos Asbestos sheets brought home from work were used in a cottage industry to repair burned out mufflers [Epler et aL 1980]. The asbestos sheets were stored in the basement where the children played and were also used to construct a tree house in which the children played. Both children developed asbestos related Hmg disease at about age 30. Asbestos cement was produced in the basement of another home for about 20 years [Otte et ah 1990]. The mother, father and one son died of mesothelioma some 40 years after the beginning of the exposures to asbestos. Lead In addition to the early report by Oliver [1914] of lead poisoning in family members of home pottery manufacture, 14 recent reports on cottage-industry home contamination and poisoning of family members by lead were found, 6 of them involved pottery. In the report by Oliver [1914], lead at up to 10,000 ppm was found in dust of potters' homes where the pottery was dipped in lead glaze in the same room in which the family lived and slept; lead was also found in the clothes of a young boy and a baby. Koplan et ah [1977] reported on six home potters and their families in Barbados and found BLLs up to 71 /ig/mL, and average concentrations of lead in dust for the six households of 2333-88,159 ppm with a maximum value of 325,892 ppm. The State of Alabama [1992] reported finding lead at up to 177,000 /tg/ft2 in a home pottery workshop where children with elevated BLLs spent some time; elevated lead levels were also found on the kitchen floor of the family's dwelling. Other studies of home pottery manufacture did not report levels of contamination, but did report elevated BLLs. BLLs up to 74 /tg/100 mL were found for children of workers engaged in ceramics (plates, cups, vases, etc.) production at home in Italy [Abbritti et ah 1979]. Molina-Ballesteros et ah [1983] found BLLs up to 98 /ig/dL in children of potters working in their homes in Mexico; and in Japan, Katagiri et ah [1983] reported lead in urine of children of home pottery workers up to 793 pg/L compared to 59.9 pg/L in control children; 112% of children of home potters had lead in urine greater than 30 fig/L. vs. 2.7% of control children. More recently in the United States, Fischbein et aL [1992] reported finding a BLL of 48 /ig/dL in a child of a home potter in New York. Manufacture, repair and recycling of lead batteries by cottage industries have also resulted in contamination of living areas and exposure of family members. Lead loadings up to 53,140 /tg/m1 were found in households of cottage industry battery repair shops in Jamaica [Matte and Burr 1989; Matte et al 1989]. Matte and Burr [1989] also found that playing in the area of the battery repair shops was an independent predictor of elevated BLLs in children. Other reports did not measure home contamination but reported lead poisoning or elevated BLLs. 46 CHAPTER 3. LEVELS OF CONTAMINATION IN HOMES AND CARS CHAPTER SUMMARY Measurements of contamination in workers' homes and cars were reported for asbestos, lead, pesticides, mercury, a few chlorinated hydrocarbons, arsenic, and fungi (Table 15). However, for the other substances reviewed as contaminants of workers' homes, data on levels of contamination have not been reported; this is true for beryllium, estrogenic substances, asthmatogens, cadmium, fibrous glass, and radioactive substances. For asbestos, there are no studies of contaminated surfaces, but in one study of the air of workers' homes asbestos concentrations up to one-half of the current 8-hr. time-weighted average OSHA exposure limit for workers were found. There are many studies of workers' home contamination by lead that document the substantial contamination that has occurred. Lead contamination of surfaces is measured either as concentration of lead in dust, expressed as ppm or as the amount of lead covering an area of surface, expressed as weight of lead per unit of area, and referred to as lead loading. When the concentration of lead in household dust was measured, average concentrations in workers' homes ranged from 1,600 ppm to 5,000 ppm with maximum values up to 84,000 ppm. In control homes, concentrations were usually less than 1,000 ppm. When lead contamination was measured as weight/unit area, workers' homes had lead loadings that were greater than 2^00 Mg/m1, ranging up to 109,000 Mg/TM1Control houses had lead loadings that were less than 1,000 Mg/TM1- Lead loadings in workers' cars ranged from 1,000 to 300,000 Mg/TM1- Control cars had lead loadings that were less than 1,000 Mg/TM1- While measurements of lead in control homes provide some basis for evaluating contamination of workers' homes, guidelines for critical levels of contamination are needed. A value of 500 ppm for the concentrations of lead in dust was used in one study as a threshold for cleaning homes. For lead loading after lead-based paint removal, 2,152 Mg/TM1 has been used for floors as a practical, not health-based level. A level of 1,500 Mg/m1 has been stated as a level of concern for children's health. In three studies of workers' homes contaminated with mercury, concentrations of mercury in air ranging from 0.02 Mg/TM3 to 50 Mg/TM3 were found. In one study of control homes, concentrations in air ranged from 0.01-1 Mg/TM3- Mercury concentrations in contaminated automobiles were 8-60 Mg/TM3- The MSHA 49 permissible occupational exposure limit for inorganic mercury vapor is SO /ig/m* as an 8-hr. time-weighted average (30 CFR 57.5001). The few reported measurements of workers' home contamination by pesticides, chlorinated hydrocarbons, arsenic, and fungi also demonstrated high levels of contamination. ASBESTOS Only one report on measurements of asbestos contamination in workers' homes was found. Nicholson et al. [1980] reported that chiysotile asbestos in 13 air samples from homes of miners and millers in California and Newfoundland ranged from less than 50 to somewhere in the range of 2,000ng/m5 to 5,000 ng/m3 (1,000 ng/m3 equates to about 0.01 fiber/cm3 [Cossette 1984]). The OSHA maximum permissible concentrations for workplace exposures are 0.1 fiber/cm5 as an 8-hr. average and 1.0 fiber/cmJ as a 30-minute average (29 CFR 1910.1001; 1915.1001; 1926.1101). LEAD Most of the measurements of lead contamination in workers' homes and cars are of lead concentration in dust expressed as ppm (or the equivalent /ig/g) or of lead loading on surfaces expressed as fig/m1 or ng/ff (1 /ig/ft1 = 10.76 ng/m1)- Similar units are used for expressing measurements of contamination of carpets, furniture, and cars. Concentrations of Lead In Dust. Concentrations of lead in house dust of control homes were reported in several studies. Baker et ah [1977] found lead at an average of 404 ppm in control homes for a study of smelter workers in Tennessee, and Rice et al. [1978] found 1,240 ppm in control homes of secondary smelter workers. In control homes for a study of ceramic workers in Colorado, Kaye et aL [1987] found lead concentrations from non-detectable levels up to 320 ppm. For a study of electric cable splicers, Rinehart and Yanagiswa [1993] found 121-879 ppm, in control homes. Watson et al. [1978] found lead at an average of 718 ppm in housedust of control homes used for a study of battery manufacturing workers in Vermont As a guideline for cleaning lead contaminated homes in Idaho, an action level of 500 ppm was used [CH,M Hill 1991], By contrast to these control measurements, Baker et al. [1977] found an average concentration of lead in house dust of smelter workers of 2,687 ppm. Rice et al. [1978] found 3,310 ppm in homes of secondary lead smelter workers, Kaye et aL [1987] found lead up to 3,400 ppm in homes of the ceramics workers, Rinehart and Yanagiswa [1993] found lead up to 1,600 prpm in homes of electric cable splicers, and Watson et al. [1978] found an average of 2J239 ppm in homes of battery manufacturing workers. High concentrations of lead in house dust were also found in other studies of smelter workers, cable workers, and battery manufacturing workers. Smelter workers' 50 CHAPTER 4. PREVENTIVE MEASURES CHAPTER SUMMARY Several measures that have been taken to prevent contamination of workers' homes and to protect workers* families are identified in the reports reviewed in this Chapter. The measures include: reducing exposures in the workplace; changing dothes before going home and leaving the soiled dothing at work to be laundered by the employer; storing street dothes in separate areas of the workplace to prevent their contamination; showering before leaving work; prohibiting taking toxic substances or contaminated items home; separating work areas from living areas of cottage industries; storing and disposing of toxic substances on farms and in cottage industries properly; preventing family members from visiting the workplace; laundering separately from family laundry when it is necessary to launder contaminated clothing at home; and informing workers of die risk to family members from home contamination and ways to prevent it. The few studies evaluating these measures indicate that they can be effective in reducing or eliminating home contamination. There have also been instances in which home contamination has occurred when one or more of these measures has been omitted. BERYLLIUM Following reports of occupational and non-occupationaJ (community and workers' families) cases of berylliosis, the beryllium industry instituted a number of preventive measures, including: engineering controls to reduce air-borne exposures of workers'; community air pollution controls; and measures to prevent exposure of family members to contaminated dothing [Eisenbud et aL 1949; Metzner and Lieben 1961]. In one plant, a double locker system was installed in 1955 which prevented removal of work dothes, underwear, socks and shoes from the facility [lieben and Metzner 54 1959], Until Newman and Kreiss [1992] reported on a case, there were no new cases of baylliosis in beryllium workers' families reported for more than 30 years. This recent case report demonstrates the dangers of any relaxation of preventive measures as the uses of beryllium, the number of workplaces where it exists, and the number of workers exposed expand. ASBESTOS Although poisoning of asbestos workers' families has been known since the report by Newhouse and Thompson [1965], and has been repeatedly associated with laundering contaminated clothing, no information exists on effectiveness of preventive measures. Belanger et al. [1979] recognized the hazard in evaluation of a factory where asbestos was used in the manufacture of floor coverings. They specifically recommended that work clothes not be taken home because this could expose others at home. Seixas and Qrdin [1986] and Driscoll and Elliott [1990] investigated plants manufacturing brake linings and made recommendations for providing protective clothing, keeping street clothes separate from work clothes, company laundering and showering before leaving work. The OSHA asbestos standards [29 CFR 1910.1001, 29 CFR 1915.1001, and 29 CFR 1926.1101] require these actions when employee exposures exceed 0.1 fiber/cm* averaged over 8 hrs. or 1.0 fiber/cms averaged over 30 minutes. In the absence of information on clothing and personal contamination levels when workers are exposed to asbestos at concentrations below these limits, the i/ adequacy of the OSHA standards for protecting workers' families cannot be judged. LEAD The report of an investigation of a stained glass window-making studio [Donovan 1994a,b], documented that the use of controls by the studio effectively prevented lead contamination of the worker's home that was adjacent to the studio. Preventive measures used at the studio included local exhaust ventilation during soldering, general dilution ventilation equipped with an electrostatic filter, adhesive mats at doorways to decrease the migration of lead dust on shoes, a laundry room located between the studio and the house that was also used as a changing room, designated work clothing that was only worn in the studio, washing work clothes separately from other dothes, prohibiting work shoes from leaving the studio, and prohibiting the child from entering the studio. Based on the results of surface-wipe sampling, which demonstrated elevated lead levels in the studio (1.2 mg/ms to 1,600 mg/mJ) but not in the home (non-detected or trace), the author concluded that the measures used prevented contamination of the home. The Lead Industries Association, Inc. has produced a video tape entitled 'Controlling Lead Exposure for Stained Glass Professionals and Hobbyists' [LLA 1994a], In another cottage industry, a home-pottery operation, the concerned potter and her family were asked to discontinue being exposed in the facility because of their elevated BLLs [Fischbein et al. 1992]. Two years later, the BLLs were normal, indicating that corrective measures, though not described, were effective. Hie Lead 55 For lead loading, the Department of Housing and Urban Development (HUD) has guidelines for floors of 200 jtg/ft* (2,152 jig/m*) and for window silk of 500 jig/ft, (5,380 jig/m*) [Jacobs 1994], The HUD guidelines are not based on health considerations, they are based on levels that can be practically achieved following lead-paint abatement These values were used by the State of Alabama [1992] and Pollock [1994], Matte and Burr [1989] cited 1,500 jig/ni* as a level of concern for children's health. CH2M Hill [1991] used a concentration of lead in dust of 500 ppm as an action level for cleaning residences. Mercury concentrations in air of workers' homes of 0.5 jrg/m3 and 1.0 jtg/m3 were used as decontamination goals in the reports by ATSDR [1990a] and Zirschky and Witherell [1987] respectively. In a recent report on decontamination of homes in Florida, 03 jig/m3 was the level at which families were allowed to return to their homes following decontamination [CDC 1995]. For PCBs, EPA guidelines for indoor solid surfaces and high contact outdoor solid surfaces state that post dean-up levels should not exceed 10 pgf100 cm* (40 CFR 761.125). Based on PCB levels found in non-manufacturing buildings, 0.11 jig/100 cm2 was used as a guideline for decontaminating a school building [Orris and Kominsky 1984], Other guidelines cited by Hartle et al. [1987] were 03 jig/100 cm1 for office buildings; for an aircraft plant, 230 jtg/100 cm* was dted for low contact surfaces, and 1 jtg/100 cm* for high contact surfaces. REVIEW OF DECONTAMINATION PROCEDURES BERYLLIUM Shirts worn for one day in a beryllium plant were studied by Cohen and Positano [1986]. Three shirts were classified as "nearly new" and three were classified as "old." One "nearly new" and one "old" shirt was laundered at the workplace. Beryllium was present at 22 mg/m3 and 30 mg/m* in the "old" washed shirt Beryllium was present at 12 mg/m3 and 20 mg/m* in the "nearly new" unwashed shirts and at 0.2 mg/m* in the "nearly new" washed shirt Although this was a pilot study, it is the only study found that provides information on laundering clothing contaminated with beryllium or similar particulate material. The study indicates that the beryllium was laundered from the "nearly new" shirts, but that beryllium had accumulated and was well entrenched in the "old" shirts. Substantial levels of beryllium dust in air were generated during laundry procedures. The concentrations were up to 13 mg/m* [Eisenbud et al. 1949] compared to the occupational exposure limit of 2 jig/m3 as an 8-hr. time-weighted average [29 CFR 1910.1000]. ASBESTOS There were no studies on the effectiveness of any methods for removal of asbestos from clothing contaminated in the workplace. One study conducted on dry cleaning a coat which contained 8% asbestos in its fabric, indicated that some of the loose fibers were removed [NIOSH 1971]. Concentrations in the air of asbestos fibers 62 longer than 5 /t that were generated by wearing the coat before cleaning were around 2/cc whereas after cleaning the concentrations were about 0.5/cc. Since the fibers were part of the fabric, the study may underestimate the ability of laundry procedures to remove asbestos from contaminated clothing. Asbestos fibers were transferred to sport coats dry cleaned with the coat containing asbestos. In a laboratory study, asbestos-contaminated carpets were cleaned for about 65 minutes by either dry vacuuming or hot water extraction, using vacuum cleaners equipped with high efficiency particulate air (HEPA) filters [Kominsky et al. 1990]. The carpets were artificially contaminated with 93 x 10* and 93 x 10' asbestos structures per meter squared (s/m1), based on levels found in carpets from an asbestos-containing building. Dry vacuuming removed little or no asbestos from the carpets whereas hot water extraction removed about 70%. An important aspect of this study was the effect of the cleaning procedures on airborne asbestos concentrations. During carpet cleaning, by either method and at either level of carpet contamination, average asbestos concentrations in room air of 0.15-0.25 s/cm3 were generated. The OSHA permissible exposure limit for asbestos is 0.1 fiber/cm* as an 8-hr. time-weighted average [29 CFR 1910.1001; 29 CFR 1915.1001; 29 CFR 1926.1101]. Resuspension of asbestos fibers was observed with a fiber aerosol monitor during a daily cleaning period of a classroom by Litzistorf et al. [1985]. Resuspension of dust by cleaning activities is an important consideration not only for the decontamination process, but also for persons living in the home and performing routine cleaning operations. LEAD No studies on laundering of clothes contaminated with lead were found. However, Simonson and Mecham [1983] showed that a workplace airshower removed from 5% to 72% of lead oxide dust from clothing samples contaminated with about 1 mg/cm1, and from 23% to 69% from samples contaminated with about 0.6 - 23 mg/cm2 in laboratory studies. A small amount of lead was blown through the clothing to the underclothing and body of the workers (up to 1% of the dust loading). Ewers et al. [1994b] studied the effectiveness of dry vacuuming for removal of lead from carpets taken from homes of children who had high BLLs. These carpets were highly contaminated with surface lead loadings of 114,000 jrg/m2 to 5,650,000 #tg/m*. The carpets were vacuumed with commercially available vacuum cleaners intended for industrial Use. The vacuum cleaners were equipped with HEPA filters and fitted with a commercial beater bar nozzle. The carpets were vacuumed 10 times for 1 min/m* each time. Surface loadings and amount of lead removed were measured after each vacuuming. After some of the earlier vacuumings, lead loading on the surface increased by up to four times, but by the tenth vacuuming the surface lead loading was reduced to 6%-61% (average 20%) of the initial loading. The 63 Author (year) Anderson [19B3] Andenon et il. [1976,1979*, 1979b] Location Industry/ Population lit Rkk P* lienon, New Jersey Amoslte worker* employed 1941-1945 In thermal imulation materiali factory Magnsnl el *1. |191 Italy Asbestos cement worker* Tiblc 2. I lollii K/Tccta of Tike-I lone Afbcttoc Giponre (Cohort Studies) Study Deafen Results Comments Cohort iludy. Morbidity and mortality among 2,218 household conlicit of amotlle workers identified. 679 of 1545 alive through 1980 were examined. Occupational, residential, smoking, medical history questionnaire administered to the exposed cohort. Vital status follow-up Is through 1980. Radiographs were taken 204 yeara after first exposure. For rsdlographlc snalysis, a frequency matched (age, gender) control group was assembled of 326 unexpoted people from the same urban New Jersey community who presented for chest radiograph 1973-1976. Retrospective cohort mortslity study of 1,964 wives of asbestos cement worken; cohort had no hlsloty of occupational exposure. Husbands employed 1930-1983; deaths occurred 1963-1986. 3/663 observed deaths were due to mesothelioma. Lung cancer overall SMR- 132 (23 observed/16.4 expected) after 20 years latency SMR* 183. Among females, there were 8 respiratory cancers observed vs. 6.4 expected. Excess risk wss confined to those with 204 years latency (8 observed vs. 4.7 expected, SMR-170. Among males with 204 yean latency, there were 12 lung cancer deilha observed vs. 6.1 expected (SMR-197). Increased frequency of asbeslot-aiiociated radiographic abnormalities among household contacts. Prevalence of radiographic abnormality aisoclated with secondary exposure was 33% vt. 3% expected baaed on the comparison population (p<0.001). Prevalence of abnormalities Increased with duration since first exposure; 40% prevalence among those with longest latency (p<0.01). Those with 104 yens of household exposure had a prevalence of abnormal radiographs of 53%. For 1971 ILO classification 1/1 and greater, a prevalence of 10.3 observed vt. 0.6% In controls. Prevalence of parenchymal or pleural abnormality 204 yean after Hist household exposure (1979b): 48% among wives, 21% among daughters, 42% among aons, and 37% among siblings. Between 1963-1988, there were 4 pleural tumors (1 mesothelioma) observed vi, 05 expected; 6 lung cancer vs. 4.0 expected. Expected based on local ratea. Among women with domestic exposure, center of the pleura was significantly elevated SMR-792.3 (93% a 215.9 - 2,028.8). Mesothelioma deaths occurred 204 years after childhood domestic exposure (2 female; 1 mate). There were 2 additional mesothelioma! among children of workers that were excluded from analysis. Dust from work clothes, shoes, hair assumed causal. No changing facilities at factory. This plant had no laundering fscllltica, and work clothes were Isundered at home. All 6 reset reported more than 10 yean of exposure. There were 2 additional mesotheliomas observed afler 1988. 145 Author (you) Joubert el al, |199l| Navntll and Tripp* |1971) Tible Z (Continued) Health Effect* ofThfce-Home Afxrtn Eapoaum (Cohort Studies) Location lodurtry/ Poputatkn ait Rlik New lamp Amoalte aibeatoa worken Czechotlovikli Chryiotile Vbeito* product procuring Study Dcrign Reault* Onaioetit* Cohort tludy. Followed houaehotd contact* of amoetle aibeitoe worken employed at a tingle facility 1941-1954. Of 4,044 houtehold contact*, 878 were examined 1973-1976. Cohort tludy, Prevalence of pleural calcification In three aabeitoa expoeed group* compared with prevalence In non* expoted reildent* or the ume area (Oroup #4). Orouo #1 800 workmen employed for more Ihin 10 yean at a factory. Prom tl 131 penon* living In the neighborhood of the factory. gMHBjfJ 114 penon* older than 10 yean who were relative* of factory employee*, Srevc-fi 8,117 pcnoill over the ige of 40 who lived in the ume diatrict a* the factory but not In the ume neighborhood aa the factory. Vital itatus followup through January 1990 Indicate* that 18% died of lung cancer, 13% died from cancer of the gutrolntettlnal tnet, end 9% died of meiothelioma. The authon ttate that cancer death* were 1 timet expected beted on national ettlmate*. Bach group wa* evaluated by X-ray for the prevalence of pleural calcification, with or without other algna of iibeiloali. Obcerved itatlallcally rignlflcent (p<0.01) Increued rlik of caldflcatlon among each aaberto* expoud group compared with Oroup #4. Oroup *1 41/BOO (3,3%) ohterved v*. 2,73 expected Proupfl 9/133 (3.8%) ohterved v*. 033 expected Orouo *3 4/114 (33%) obiervtd v*. 039 expected OrouP < 18/8117 (0,34%) Some figure* reported la the ptperteem contradictory, Thl* ippean to be additional follow up of the Andenon et al, atudle*. In group dl, 3 were alio relallvea but were counted In group d2 rather than group #3. Blood relation* were auumed to have Increued expoaure due to contact with worken wearing contaminated work clothe*. 146 Author <r> KJlbum ct al. (1985,1986] Locution/ Indinby/ Population at Rhk Lot Angelca County Shipyard worker) Table 3. Health H/Tccti of Tko-l lotne Aabeatoa Eiponue (Community Studiea) Study Dealgn Rrcuttc Comment) Community-bated cohort. Prevalence of radiographic evidence of atbeato* among thlpytrd worker* and their houtehold contect) with at lead 20 yean latency (n*10t7) wat compared with that of 2 previouily atudied comparicon group) (Long Beach cemut tract and Michigan adult)). Medical and occupational hlclory obtained by domination and Interview. Prevalence among houtehold contact) wilhoul occupational expoaure wat reported. Among 274 wive) of thlpyard worker), 11.3% had radiographic evidence of arireatoait (profution 1/0 or greater), compared with prevalence of 0.6% In the California and 0.0% In the Michigan eompariaon group), Prevalence Increned with time tlnce tint expoaure; the prevalence rate among thoae with longed latency waa 32%. Among 140 female children, the prevalence rale Ml 2.1%; a prevalence of 7.6% wat obcerved among 79 torn of ahipyard worker). Poulble (election bio rtiulllng from volunteer dudy participant). No difference in prevalence obterved by amoking ilatua. Mod ihlpyard worker) had indirect (bytlander) expcuure. Famillea of imulaton appear to be at Increared rlik of acbeiloali compared with other ahipyard worker). (1% of ahipyard worker) were Iniulaton; about 25% of atbettoalt In worken' famine) occurred In famillea of iniulalora.) 147 Author (year) Newhoute mil Thompeon [1*3] Vienne end Polen (197BJ Table 4, Health Effecti oThb-HoM Aetata Eqain (Cuae-Control Studlen) Location London, England New York Slete Indmtij/ 5tudyDec(gn Population at Rkk Hoepltel-bleed Population-baaed Metched ceee-conttoL Ceeee (n-M) were lutopey aerie* who died of meaothellom* (pleurel end peritoneal) 1917-1964; metched on gendet end birth date (/ J yean) to in-patient control* from him hoepltel who were hoapltallxed 1964. Two other comparieon group* were uced to verity reiulta, but not reported In paper 1. matched on gender, birth date, end date of admleelon, end 2.17 petlenla from ume hoepltel pathology rente who were mledlegnoced it meaothelloma. Matched caM-control. Carer were 5Z <30 pleural/20 peritoneal) hlrtologltally confirmed female meeothelloma (pleural and peritoneal) death* <1967 1977); one-to-one matching on gender, race, county of retldence, marital atalur, age and year at death; controli died from caurea other than cancer; occupational hlatoiy by queatlonnilre, medical and Induitrial record). Reaulta Comment* 9/76 cate* (7 female; 3 male) reported domeatlc exporure compared with 1/76 control) from the Inpatient Krlea, Moat female expo*urea from laundering work clothe*; 2 male* expoaed In childhood to family member* who worked In atbealo* factory; latency ringed from 16-33 yean. Relative Riik from matched pain analyala for domeatlc erpotur* (included 3 with occupational expoaure) repotted u 10 (9S% a-lA-37A). Analyala on aubiet of 46 nonoccupationally expoaed cue*: 8/46 reported domerllc expoaure va. 1/46 control) (p 0.02). All 10 domeitlc cite* expoaed during hand laundering of work clothe*. 148 Table 4. (Continued) Health FJTecti of Take-1 ioroe Axbcatoa Exposure (Caae-Conlrol Studies) Author (year) McDonald and McDonald {19801 Loolion Industry/ Study Dolpj Population at Risk Reeutts Comments Canada and USA Population-baled autopay aerlea (Canada 1960 19721 USA 1972) Matched cate-control. 557 pleural and peritoneal mesotheliomas with autopsy; matched on hospital, gender, age, and year of death to controls with pulmonary metastasea from non-pulmonary primary who were auloptied; occupational, residential, smoking, and non-occupalional exposure histories from interview (blind) with relatives for 490 matched pairs. Occupational exposures coded blind and cumulated to 10 years before death of case. B/357 cases vt. 2/357 controls reported domestic exposure to asbestos dust on work clothei of household contact (p-0.08 for matched pain analysis). 3/8 ron-occupational cases nd 2 controls were exposed to contaminated clothing In childhood. 3/8 cases and 1 control were exposed to clothing of a chrysolite production worker; 3 cases and 1 control were exposed to contaminated clothing of insulation factory workeia. Whltwell ct al. |1977) England Hcnpital-baied Case-control. Asbestos fiber content in lunp of 100 consecutive pleural mesothelioma autopsies compared with 100 lung cancer cases and 100 lunp of people who died from causes other than industrial lung disease or lung cancer for whom occupational histories were available. Occupational and residential history obtained from patients or relatives. 1 mesothelioma reported in asbestos worker's family. Although not explicitly slated In published report, apparently no casea were observed In either control teriei In asbestos workers' families. Esther worked In gas mask production and brought work home. Lunp or his son had 30,000-100,000 asbestos fibers/gram dried lung tissue. 149 Table 4. (Continued) Health Effects of Tike-Home Asbestoe Eqmeuro (Cue-Control Studies) | Author (jtir) Location McEwen et al. |1971| Scotland Rublno et *1. |1972| Italy (Piedmont) Aiheroft and Heppleston (1970) Britain Induatry/ Study Design Population at Rick Results Comment! Popula lion-bated Matched cate-conlrol. 83 metothelloma catet who died 1950-1967 from ail pathology department! In Scotland. Two control group! were matched on age and gender to the nearett chronologic pathology report from the lame hoipilal: (1) coronary trteiy dlteate deathi, tnd (I) lung and gastric carcinoma catet were matched to pleuril and peritoneal metolhelloma diet, reipectlvely. Varlout Industries; Piedmont produce! only chryiotlle Care-control itudy of 50 confirmed cuei of pleural metolhelloma admitted to 2 Turin clinical aeltlngt 1960-1970. Controls were 50 patients from the tame lneiitutlon metched on gender and age. Shipbuilding Cate-control itudy of 23 catei of metothelloma (20 pleura, 3 peritoneum; 19 males, 4 females) that came to autopiy compared with 46 hospital control! matched on sex and age, free from malignant dlieate, Only a few catei and control! had ihared houteholdt with aibeitoa worked. No itatlitlcaily ilgnlllcant dlfferencei between theie two groups. The number of nonoccupitlonil cuei wai not reported In the publication, The cite of a woman who wathed the clothes of her hutband who wii a dockworker li detcribed. 12% of metothelloma reported In Ihe cate terlei were In worked' family membedi 3 catei (2 men and 1 woman) hid lived with pcnoni employed In the aibeitoa Induitiy, compared with none In Ihe control group. The wife of a man worked In Ihe aibeitoa industry, and 1 woman's brother worked In an aibeitoa cement factory. Occupational expoiurt wai unequivocally demonitrated In 3 men. Aibeitoa bodies wert found In only ont cate. 91% of the catet had a hltlory of exposure to aibeitoa vt, 41% of 46 matched contrail (p <0.001); 1 of the citei tciulted from domeitlc expoiure. A widow of an aibeitoa worker wai cxpoied for 3 yean to aibeitoa dull brought home on her huiband'a clothes, halt tnd shoes. Ptpcr Includes table of fiber and aibeitoa body counta. 150 AUTifOR(S) (YEAR) COUNTRY INDUSTRY Rusby [1968] England Asbestos Teystter and Lesobre [1968] Asbestos Champion [1971) Canada Knappmann [1972] Wait Germany UIHngton et 1. [1974J USA U el al. [197B] USA Epler et at. (1980) USA Atbetloa Asbestos Asbestos Asbestos Asbestos Rlibcrg et al. [1980] USA Jorgensen [1981) Oenmarlc Construction Asbestos (iniulatlon work) HEALTH EFFECT T^bleS. Health Effects of Take-Home Asbestos Exposure (Cue Reports) CASES/RELATIONS!{IP AGE(S) AT DEATH OR DIAGNOSIS COMMENTS Mesothelioma 1 Female 71 Asbestosis Pleural plaques Case report of asbestosis in a man exposed as a teen to his father's work dolhes worn home from an asbestos plant. Mesothelioma 1 Mate 31 Mesothelioma Familial mesothelioma Man lived for several years wilh sister who was an asbestos worker who came home wilh dusty clothes and hair. 1 Wife 66 52 Familial mesothelioma 1 Mother, and 1 daughter 51,34 Pleural changes Mesothelioma 2 Wives of asbestos workers I Brothers 60^6, 33 and 27 Familial pleural and peritoneal mesoihelioma Father, I brothers and 1 sister Pleural plaques 3 Wives of insulation workers 61,71, 60, and 52 71,54 and 58. Woman laundered clothing of 3 daughters who had worked In an asbestoa factory for 1-2 years. 26 year latency. May also have had environmental exposure since he lived near an asbestos plant Tor 2 years. Father was a pipe lagger and had asbestosis. Son never had occupational exposure. 42 yean from beginning of exposure to onset of lumor. Domestic case resulting from residence in the same house ss an asbestoa worker who died of mesothelioma. Father was shipyard Insulation worker who had asbestosia and died of lung cancer, His wife and eldest daughter died of mesothelioma. Wife laundered dusty work clothes, Wives were involved with cleaning husbands* clothes resulting in mesothelioma in one and pleural changes in the other. Brothers played as children In room used as muffler shop. Both developed pleural changes In young adulthood, although changes in one could have been related to subsequent occupational exposure. All cases smoked. Father died of peritoneal mesothelioma. The 2 tans and their sister died of lubuto-papillary mesothelioma. No asbeslos industry employment; father and sons worked in construction industry. Exposure was limited to laundering of clothes, dusty shoes, etc. Of the 3 women, 2 smoked and 2 had other relatives who were insulation workers. 151 AUTHORS) (YEAR) COUNTRY Martenuon tt l, (I984b| Sweden Kroutcl et il. (1986) USA Magee et al. (1986) llaly Huncharek el at. |1989J USA U et al. [1989| USA Olie el al. [19901 | Denmark INDUSTRY Asbeitoa (foundry) Table 5. (Continued) Health Effect* of Takc-Hone Asbestos Exposure (CUe Report*) HEALTH EFFECT 4 CASKS/RjELAITONSHIP Familial pleural mesothelioma Sitter and brother AGE(S) AT DEATH OR DIAGNOSIS COMMENTS 51,58 _ Brother dead, slater survived. Father's work clothes hung In kitchen when they were children. Aibcetoc Familial pleural mesothelioma Mother, ion and daughter of a lumber and shingle company worker. 74, 40, and 35. Son was only one with possible occupational exposure, but diagnosis at age 35 suggests childhood exposure. Chrysolite ore Mesothelioma Single male case. 41 Indirect exposure to asbestos from Canart Mine in Conics. contaminated Exposed as child in pub in house. Analysis of lung mineral with Iremollte content showed chrysolite at background and elevated levels of and attlnolite. tiemolite and actlnolite asbestos. Fiber sise and mesotheltal carcinogenesis discussed. Paper contains data on lung fiber burden. Albedo* Pleural mesothelioma Single case (female) 76 Indirect exposure to husband, a shipyard machinist, who dismantled boiler* and other related machinery for 34 yean. She laundered his clothes. Paper contains data on lung fiber burden. Aabeatoa Familial mesothelioma 2 Female catet. Father worked in aabeatoa plant. 32,49 Cotton cloth aacki In which molded asbestos Insulation had been transported had been used to make diapen for children. Results were the deaths of the mother, a sister, and a young unde who lived there and worked as insulator. In addition, the father died of asbeslocla. Mother laundered asbestos-contaminated diapen and work clothes. Amocite atbedoc cement Familial mesothelioma Family cluster of 3 deceased. 74, 79,45. Family produced asbestos cement In their home. Used dry hand mixing procedure. Mother, father and a son died of mesothelioma; 2 sons and a daughter survived. All decedent! smoked. 152 AUTHOR(S) (YEAR) COUNTRY -- Oem et *1. (1991) Norway Anonymous [1993b) Bn (land INDUSTRY Table 5. (Continued) Health Effect* or Take-Home Asbestos Exposure (Case Reports) HEALTH HPIUCT # CASUS/R]!IATIONSIIIP AGE(S) AT DEATH OR DIAGNOSIS COMMENTS Asbestos (various) Pleural mesothelioma 1 Woman Asbeslos Pleural plaques 3 Daughters 79 63,62 60 Family made up of 2 brothers, a ilsier and her husband. All males were asbestosis Insulators and 2 were smokers. Oldest brother (alive) has asbetlosis, Other brother and sister died from mesothelioma. Brother-in-law died from cancer bronchiale. Woman cleaned asbestos-contaminated work clothes. Daughters of pipe lagger. Exposure was laundering of work clothes; 2 younger daughters were asymptomatic but all 3 had varying degrees of pleural plaques. Father died of peritoneal mesothelioma. 153 AUTIIOR(S) YEAR COUNTRY INDUSTRY Lleben and Platiwfca [m7] USA AlbCItC* (Iniillation, ihlpbullding) Dilquen et al. [1*W| Germany Albeitc* Heller cl al. (1970) USA Aibeitoi Bltienohl and Ou [1971] Germany Aibeitoe (Imulatlon and producli wch at cord), wall, plalct, etc.) Tkble 6. Health Effect* of Itte-Hooe Aabeato* Czpocure (Cue Seriea) HEALTH EFFECT /RELATIONSHIP AGB AT DEATH EXPOSURE COMMENTS/ ISSUES Meiothetioma: 1 pleural and 2 peritoneal. Pleural plaquei Pleural metolhelioma Pleural merolhelloma Syearold girt whole hiher worked with aibeitoi Iniulatlon. 40-year-old woman whoce lather and brother were aibeitoe intulallon workert. 67-yeir-old woman whoce two com were ihlpyard aibeitoe (mutation worken. 22 caiei among domeitie conlacli 1 woman. Waihed pipefitter hueband'i aibeiloKonlaminated work clothe*. 1 woman wbote hulband wai expoaed to aibeitoi Imulation at a chemical plant. She laundered hii work clothe*. 3,40,67. No numerical exposure data given. Of 41 metolhelioma caiei reported from 132 Penmytvanla hoepttete 1938-1963, 3 were family member! of ubeitoe worken. 113 cetea of pleural plaque* and 143 catea of aabeitoala from the Hamburg area are reviewed. Of 92 caiei of pleural ptaque* with a hlitory of expoture to aabeatoa dull, 34 were occupationally expoaed, 22 domeitleatly, 21 by urban dwelling and 10 by mutllple came. 3 had no hlitory of ubeitoe expoaure. The latency period for plaque* wai 40.2 yean. Btpoiure data given In termi of Bail German itandard. Radiological review of a teriet of 10 caiei of pleural meiothetloma aeen at Maiuchuutti General Hotpital 1960-1967,1 cue ml the wife of an aibeito* worker. 1 26 catea of pleural meiothellomu from II chemical plant* In the district or Metxeburg, But Getmany. Thli group 1* made up of 22 patient* from the Leuna Chemical combine, 2 pallenti from the Beuna Chemical Combine, 1 patient from a metal foundty, and 1 cue In the wife of a chemical plant worken. Chemical plant worken were expoaed to atbeilo* imulatlon. All occupational caiet had been expoaed to duit level* exceeding the Bait German Hand*id. Thli group Include* worken not directly working with ubeatoe, but working nearby. Of the caiei, 46% occurred after retirement. 154 AUTHORfS) YEAR COUNTRY Vlannt et el. (19S1) USA INDUSTRY Six New York countie* 1 Orundy and Miller 1 [irm 1 USA U.S. population-bated Oreenberg and Divlei [1974) Engltnd/Wilea Atbeitoa Milne [M76] Auitralla Aabcttoa (aibeatoe/eement) Edge end Qtoudhury [1J7B1 England Aabeitoe (ihlpyard worker*) Tkble 6. (Continued) Health Effect* of Thko-llome Axbeitot Expoeure (Cue Settee) HEALTH EFPBCT #/RELATIONSI DP AOE AT DEATH EXTOSURE COMMENTS/ ISSUES Mcaolhelloma Childhood meaolhelloma Meiothelioma Metothellom* Pteural mesothelioma Or 7 cue* of Indited expoaure, 6 wen femile*. IS cam of childhood meiothelioma In US children. Age tenge; 4 through 17. 2 women with meiothellomii uodilcd with houiehotd expoaure of 2 and 3 year* duntlon; 1 woman'* huiband worked In an atbealo* factory, and 1 wai erpoted to her brother'* work clothe*. 1 can In a woman who** father worked In the atbedo* cement Induitry. No expoaure In the ertei bepn after 1943; length or expoeure ranged from 6 month* to 30 year*. 1 woman married to ihipyird plumber who may have brought duat home on clolhet. Population-baled Incidence ttudy (cate Kriet). Detcripllv* autveyof 31 (12 male; 9 female) hlaiologlcelty confirmed meeothelioma cate* diagnoted 1973-197*; occupational hlaloriea from caae* or relative. No control group. U.S, populitlon-beaed death certificate aearch. No expoaure hlitory, although occupational hlatory of aome fathen contlatent with ibeato* expoaure. Apparent ihort latency In children compared to adulti. 1967-1968 meiothclioma cate aerlei (n-413: 3SS pleural; 4S peritoneal) from populationbated reglitry. Aabctloa expoaure hlatoty obtained by Interview from ceaet, relative!, employer* and workmatea. For 246 of the 413 ciaea, the dltgnoala wal hlatologictlly confirmed. Retroipectlve rurvey of 32 caiei of metothellom* In Victoria, Auitralle. 771**0 uihore found occupetlonal hlatoty equally effective at an ubeatoa body count to Indicate paat expoaure, In 16% of cite*, there we* no evidence of expoaure to etbeitoa, and 2 caret of peritoneal cancer were In tlbllnp without aibertot expoeure. 47 men end 3 women dlegnoaed with pleural meaolhellomi 1966-1976 among 64,000 realdenla, 7,000 of whom worked In ihip conitruclton. All 30 cate* of pleural meaothelloma htiiologtcatly proven and accepted by Pneumoconloai* Panel All men plu* 1 women occupationally expoaed; 1 woman expoeed at home, another had no known expoeure. Aibcrloa content of latt 20 caua wai meatured; 18 catei aubitanllally exceeded that of the general population. Metaalaaee, frequent nl necropay, occurred In 23 of 47 caici tutoptled. 155 AUTHORS) YEAR COUNTRY Blanchl et al. [1982] Italy Blanchl ct al, [19871 Italy Blanchl et al. [19901 Italy Blanchl ct al. [1991) Italy INDUSTRY Asbestos (shipyard work) Tkble & (Cootintied) IlealIh Effect! of Take-Home Aibeatoe Exposure (Owe Series) HEALTH EFFECT #/RELATIONS! DP AGE AT DEATH EXPOSURE Pleural tneaolhelioma 1 woman whoae huaband waa a thlpyard worker. Aabeiloa (thlpyard, codturn carbonate factory) Hyaline pleural plaquee Shipyard, sodium carbonate factory, textile, artisani, domei tic meIda) Hyaline pleural plaquee 59 caaea were attributed to domeatlc expoaun (laundering aabeatoacontaminated work dolhca of family memben). 9 caaea with occupational and domeatlc expoaun. Not elated Pleural plaquea al necropay were found In 55% of 121 women with hlalory of domeatlc expoaun. Shipbuilding, todium carbonate factory Aabcttot bodlea Hyaline pleural plaquea 1,765 necropalei (1,127 men; 638 women). In women, cleaning of work dothei polluted with aabeatoa waa the main source of expoaun. Domeatlc expoture reaulted in pleunl plaquee In about half the necropsies on female pitienta. COMMENTS/ ISSUES Of 70 caaea (64 men; ti women) teen at Institute of Pathological Anatomy of Trieste 1967-1980 1 waa due to probable domeatlc expoaun. Necropsy findings available In 63 caaea. Remaining 7 caaea were diagnosed at thoracotomy. Of the caaea, 43 employed fn shipyards, moat prior to 1940. Intervale between fiist expoaun and death ranged from 28 to 61 yean. Aabeatoa bodies found In 48 of 61 cases. 74 women with hyaline pleural plaques found at necropsy. 2 caaea with occupational exposure. Sufficient expoaun data could not be obtained on 4 caaea. Pleural malignant mesothelioma waa noted In 2 cases with a history of household expoaun, 1,620 necropaiea (1/140 men, 580 women) wen performed from Oct 1979 to Dec. 1987 In Monfalcone, Italy. 121 women with hlalory or domestic expoaun wen compared to 57 women with no hlalory of domeatlc expoaun. Pleunl plaques were significantly more prevalent In thou women with domeatlc exposure (p<0.001). The prevalence of hyaline plaquea waa higher In every occupational category for women with domestic exposure than for women without domeatlc exposure. Prevalence of pleunl plaquea and asbestos bodies varied by occupation In men; the highest prevalence was In those who hid worked in the sodium carbontte factory. Only 21 of the 638 necropaiea on females had a history of occupational eapotum. 156 1 AUTHORS) YEAR COUNTRY Blinehl et at. (19M| Italy INDUSTRY Title d (Continued) Health E/fect of Ttke-Iloroc Aibettoa Bipoaure (Cue Setka) HEALTH BFPECT d/RELATIONSHIP AOBATDHATH EXPOSURE Aabeatot (ihipyard, lodlum carbonate lartor) Muothelloma 6 women had hlatory of domeitlc expoaure (laundering aibeitocconlamlnated clothing of family member*), Landet and Vlakum |1983! Denmark Atbettoi work Olbba cl al. (1989) Walci Aabeilo* Pleural plaquti, Pleural celclltcetkm, Pulmonary flbrorli, Aibeatotla Pleural meiothetloma Of 63 women (tpouiei of worker* expoaed lo atbeiioi) wlih Indirect (non-occupatlonal) expoaure lo aibeitoa, 9 (17%) had radiological changea characterblk of expoaure to aabeito*. Expoaure oomiited of laundering aibeatoi-conlamlniied work clothei. Adult women 1 male and 11 female* with non* occupational expoaum (Zielhuli group II, e.g., the wlvei of eabeatoe worker*) included In the itudy. 47-72 COMMENTS/ ISSUES 92 malignant meiothellomai were dlagnoaed between Oct. 1979 and April 1992 at Monfalcona Hoapltal. 63% of Iheae were aaaodated with domeitlc expoaure. 73 caaei had occupational Malory of expoaun lo aibeitoa. One cate had a hlitory of probable environmental exposure. The reieirchen attempted to enroll 113 ipoutet of aabeitoa-expoaed worker*. 90 participated In the iludy, 20 were excluded due to lack of expoture (X-ray* were normal), 3 wen excluded due lo occupational expoture (one had pleural plaque*), 2 were excluded for other pulmonary dlieaiei. 84 ciiei dlagnoaed 1979-t9B6 chocen became the hlitory of aibeitot expoture wai abaent, indirect, or Ill-defined. 3 purpoeet erf itudy were: 1. correlate lung mineral count with Ziethuii (1977) occupational expoaute grouping*; 2. determine whether any metothellome* wen unrelated lo atbeitoe expoaute; and 3, compafe the cote erf amphlbole* and chrytollle In cauutlon. Conclude that; 1. Zielhtua method loo complex; 2. meaolheltomii may develop in tbtenct of eibcatoe expoaute; and 3. amphlbole* are more Important than chrytollle. Electron microacope mineral fiber enelyil* data provided by expoaure group, 157 AUTHOR(S) YEAR COUNTRY Olbbi et il. [I9M| Water Klondike et at. [1990| Oermany KMIuoto [19M1 Finland Martenrron et al. [1964a] Skier et al. [1987] U.SA, INDUSTRY Thble 6. (Continued) Health Effectr of Thke-Homc Arbeataa Etpoaun (Caae Strict) HEALTH EFFECT //RELATIONSHIP AOB AT DEATH EXPOSURE Aibeitoe (thlpyard work, lagging, building, ordnance) Malignant pleural merothctloma 10 cater In family memben, 9 of whom were (pouter of acbecioe workerr and 1 war daughter of a man who died of atbettorlt. Age range; 47 to 72 Albertoa Arbeitoi Arbetloa work Inrulatlon work Aibetloala Merothelioma 48 non-occupitlonal reglrtry cater of merothelioma and 19 carer of aiberiotlt (11 male; Si female). 10 of there lived near an atbettot plant. Pleural plaquea, Pleural adheriont, Pulmonary fibred!, Metolhelioma, Meaolhellotna Radiographic pleural changer (ptaquer, calcification, thickening) 4 carer of irbertoeei In 4 rltlerr whore father had been occupationally expand ta mixed dutti. Women who had been expoced lo (bettor during childhood vie her frther't work dottier. 18 (19.4%) wlvet of arbertoi-expoced Inrulatlon workert rcrecned had radiographic abnormaltiler. COMMENTS/ ISSUES Thia waa a companion or typer of lung flbcn and riie dlitributlon in a wrier of nonoccupetiontl carer of merothelioma with a teriei of known occupational expoaura In female gat mark workert. The non-occupatlonal group fiber exporuie wu variable; 6 thowed high croddolite; 7 allowed high emorite; 1 high ehryxotlle; and 2 rhowed normal for all fiber (reveral thowed more then 1 high fiber group). Confirmed report! that even In the nonoccupetlonel area, atberlot reprerentr a nonnegllgible rltk for direaaea of the lung Nonoccupational tirk facton identified In ihtr tudy Included; laundering (46%); ure of atbeiloa containing material! In the houre (21%); and telrure acthdtier (1S%). The Talher 50 yean earlier had been occupationally expoaed lo mixed duttt and prcaumably brought them home on hit dother. Analyili of 32 crcer of mallgntnt metolheliomi. All but one care wu occupallonai. 117 wlver of arbertor-expored Iniulrtlon worken were tcreened with X-rayr and pulmonary function lertt, Nona of the 24 women under age 40 hid any X-ray abnormalities Exporure for all of Ihem wu leu than 8 yean. There 24 were excluded. 18 (19.4%) of the remaining 93 had radiographic abnormal!tier. 158 AUTHORS) YEAR COUNTRY Olireltl tl *1. (1992] Inly INDUSTRY Aibeitoa (ihlpyard) Table (. (Continued) Health Effecta of TUc-Hame Aibeatat Expewre (Cue Settee) HEALTH EFFECT #/RELATIONSIHI* AGE AT DEATH EXPOSURE COMMENTS/ ISSUES Meiothelloma 5 women with hlitoiy of domettle eitpocure to aibetloa (laundeitng the aibeiloa-contamlnated ciolhlni of family memben). Age at death of all taut 31 to n yean (median 70 yean). 170 pteunl metothellamai examined at necropty between 1968-1987 (Trieile Unlvenity), Occupational hltlorlea continent with aibeato* expoeurt In ISO catet. S had no aibeitoa expoture hlitoiy but lung tediont ihowed atbeatoa bodlet. S women had a hlitoiy of domctllc expoture to atbeatoa (laundering the aibeitoc-contaminaied clothing of family memben), 159 Author [year] Location Contaminant Bath for Study Bohne and Cohen (19M) Ohio Beiylllum Chambeiltn ct al. [I7] Pennsylvania Betylllum Cheaner [1950] Ohio Beryllium Cohen and Poaltano [1986] Ohio Beryllium Elaenbud el at. (1949) Ohio Beryllium Anderson et al [1979b] New Jeney Albeit oa Tibia 15, Woriceit' Home Conlaminatfoo-IodustTUI Hygiene Aspect* Prone* Beryllium production Beryllium plant Beryllium plant Beryllium refinery loduetitaj Hygiene Methodology Industrial Hygiene Observation Qmunenta oc Rccommerulattoca Fabrics exposed at worlcille. Electrostatic charges Increlied fabric contamination of cotton, but not Nome** fabric loading up to 2,800 pg/m2, 5 patient* were family member* of beryllium worken and cleaned their duaty clothe*. The authors slate: The Introduction of proper Industrial hygiene metiuret htt evidently reduced the number of newceaet of chronic granulomatous pneumonitis due to secondary transfer, since none ha* been aeen by u* for the put three yean.' Cate hlitorlet of chronic pulnvonery grsnulomilotls Woman used empty beryllium ore bap for dlth clothe*. She got the bap from * neighbor who worked at the plant. New and uied ahlrta worn at work were analyzed for beryllium In the fabric. Fabrim were agitated In glove boa to measure re-suspended beryllium. Beryllium concentration* ranged from 12 to 37 mg/m2 In unwathed shirt fabric. Air concentration of beryllium measured In refinery wa* only a fraction of the PEL of 0.002 mg/nr. The old ahlrta alto showed significantly higher concentralIona of betylllum and resuspended significantly higher quantities of beryllium to the elr than newer ahlrta. Concentrations of resuspended dust from old, unwiahed ahlrta up to 0.64 pg/m3 were found. Beryllium production. Amoalte aabeatoa product menufactuHn( Study of dust generated by laundry procedures using 100 uniforms worn Tor one day by plant employee*. Air concentrations of beryllium: shaking tolled clothe* O.l-l.l mg/m3; scrubbing 3-7 pg/m , shaking and folding wished clothes 4-6 pg/m3. Estimated Inhalation dote during tingle home-detnlng of work clothes was 17 pg of beryllium. Evaluate health atatua of 679 homehold contact* of aabetlo* worker*. Interview*, X-rayi, physical exams. Family contacts had no other known aibesiot expoeuro. 33% of household conuclt hid radiographic abnormalities v, 5% of controls. Plant did not have change room* or change or clothing available; dothci were washed at home, 184 Author [year] Location Belanger et *1. [1979] lUlnoli Oontamlnant Dadtfor Study Asbestos Blanchl et a). [1987] Itaty Drlicoll and Eltloll [1990] Michigan Asbestos Aibeiloa Olarelll et al, [1992] Italy Aabeitoa Qlbbt et al. [1990] United Kingdom Huncbarek el al. (19S9| USA Aibetlot Aibeatoa Table L5, (Continued) Worker*' Home Contamination-Industrial Hygiene Aspecta Prooctt Industrial Hygiene Methodology Industrial Hygiene Obuervulkm Comment* or Recommendation* Vinyl aabeitoa & alpha II aabeitoa floor covering manufacturing Penonal A area sampling Separate locker* for dean and dirty clothea, Coveralls provided. Showers provided. Recommendations were made to change clothea and leave all worh clothes at work. Specifically, work clolhei mutt not be taken home lo be washed as this coutd expose others at home, Aabeitoa related Industrie* Interviews to determine occupational histories and practices of washing clolhei at home. For women, cleaning work clothing was the msln source of esposure. Many women were exposed In this way for more than 20 year*. Manufacturing of aibeitoi brake Ilningi; production of adhealvei, lealcrt and palnti. Vacuumed aamplea of work clothea and car seal via phaee contrail microscopy (PCM) and transmission electron microscopy (TEM). Vacuum Samples: all clothing (n*7) was contaminated with asbealoa, 4 of 6 aamplea from worker* car acata were contaminated with asbestoa. Recommendation Included leaving contaminated clothing at work and showering before leaving. A variety of work performed by shipyard worker*, dock worker* and aaiton Review of 170 clinical cases In which necropsies were performed. 3 cases had domestic exposures lo ssbcsloi In cleaning the work clothes of their husbands who were employed in shipyards. Shipyard, lagging building and ordinance work Study of 10 non-occupations! cases or mesothelioma 9 cases were due to exposures to asbestos from washing husbands' work clothes. Exposure of ipouse to contaminated clothing for 34 yean. Post mortem fiber count* from removed lung Fibera/g of wet tuna tissue: OiiysotUe 1.72 x 10* Amodte/ctoddollte 39 x 10 Tremolite/actinolile/anthophylllte 221 x 1QJ. Husband was a shipyard machinist whose work clothes became covered with dust. His wife regularly laundered these clothes at home, 185 Author [jear] Location Komlntky ct el. |1W) Ohio Gbfltuninut Baik (or Study Aiheitoa NIcholMxi et tl. [1980] California A Newfoundland NIOSH [1971] Ohio Aabeataa Aiheitoa Sawyer [1977] Connecticut Aabeatoa Selxu and Oidln |1986| New Jertey Aiheitoa Abbrittl et at. [1969] Italy Lead Thble 13. (Continued) Worker*' Home ConUmlnatioo-lnduatrU] Hygiene Aipccti Proceaa Industrial Hygiene Methodology Inrfuatrial Hygiene Observation Cbtnmetrt* of Rocoaunembdoan Wet ft dry vacuuming to remove atbealoe fiber* from contaminated carpet* and determination of airborne level* during vacuuming. Worker*' home contamination from mining and milling atbeaio*. Trammlulon electron mlcroicopy wai uied to analyze air lampte* collected during vacuuming. An EPA method wai ured for analytic of carpet temple*. Carpet* contaminated at 1 million and 1 billion atbeito* ltrudum/ft3. Decontamination by HEPA filtered dry vacuum and hot-water extraction cleaner*. Air aampte* were collected In home* of atbeitoa worker*. Wet vacuuming reduced carpet contamination by 70%. There mi no lignlfieant evidence of change following dry vacuuming Air concentration* Increued 2-4 time* during vacuuming compared la ptevaeuumJng teveli. 13 Chryaotlte aibeatoa aimptea ranged from 30 to > 2,000 < 3,000 ng/m3. There an the only mearurementa of aibeatoa concentratlona in worker*' home*. Launderlng-trantfer or fiber* to other clothe* and cleaning aolution. Laundry Brake ihoe manufacturing Ceramic factorial ft workahopa at home An aibeitoa-containing coat (B% aibeatoa) waa dry cleaned with non-ubeato* containing clothe*. Air aamplet collected on membrane filler anelyied by phete content mlcroaeopy. Samplet collected In building laundry, not hornet. Work clothing mi vacuumed u employee* left work and duit wit analyzed utlng polarized light mlcroaeopy and X-ray diffraction. Sampling of houae dual. Methodology not reported. Demonatraled aubitantlal (rtntfer of liber* to other clothe* and to the dry cleaning fluid. Aabeato* flbera/cm3: Picking up clothing Loading waaher Loading dryer Peraonat 04 0.4 0.0 0.4 (up to1.1) In Chin abate* abatement project, controt* wen lubatantiel to them era probably minimum eitlmatei of many home laundry eitpotumi In Ihe peat, Clothe* only worn for 4 hour*. Vacuum ample* from *11 work clothei contained chiyaotlla aibeatoa fiber*. Quantitative data not preaented. Potential for home contamination via dothea brought home by the worker*. Provide dean uniform or dlapoaable one* to all employee*, Separate lolled work dothea from alreet clolhca. Mean lead concentration* in houae duit were 2.7 and 4,7 mg/m3 where worker* were expoted in facroriea and where workihop* wen adjacent to houtea, mpedlvely (va. 0.8 mg/m3 (n contrail). 186 Author [year] Location Ape! and Sings 1 (1980) Alaska Contamloaot Basis for Study Lead Baker et al. [19771 Tennessee Barnett [1994] Oregon Bamett [1994) Oregon Carvalho cl al. |WM| Bruit Lead Lead Lead Lead CH2M Hill (1991) Idaho Lead Cook et al. [1993| Colorado (Leadville) Lead Qachur e< a!. [1995] New Jersey Lead Table 15. (Continued) Worker*' IIoom Cootaro)tntfoo-Induttrial Hygiene Aspects Pfoctfla Industrial Hygiene Methodology Induttrial llygfene Obaeration Comments or Recomoendatioo* Lead acid (forage battery manufacturing Air etmpllng In plant Pereonil breathing zone templet (5) ranged from 111 lo 1,053 pg/m3. Owner A family lived above plant. Recommended; Installing change room, doting up hallway between plant and home, clean home, and monitor family for lead espoaure. Secondary lead imelter Sampled homei for lead content in houte duii. Analyzed wipe iimple* by anodic a tripping vottamelry. Dust in worken' hornet contained lead at 2,687 ppm (< 1,000-80,000) vs. 404 ppm for controls. A* a result of study, workers hornet were cleaned. Worken started showering end changing clothes before going home. Tile manufacturing Not applicable 1 worker had a blood lead level of 73 pg/dL Investigator* think at kail one child (of worker) hie high blood lead, Bronze foundry Not applicable. 2 children of foundry worken hid high BBLs (14 A 23pg/dL). Oregon OSHA documented that employee* were taking lead dust home on dolhet. Lead imelter Blood lead aamplci analyzed via atomic abrorplion ipectrophotometry with healed graphite furnace atomizer. Children of lead worken had higher blood lead values (67.5 pg/dL) thin other children (56.6 pg/dL). Lead worken took used Villen* home from the plant, for re-use in their home. Lead imelter Vacuuming and shampooing, nalyiei for lead and other metali. Lead loading In carpel* ranged from 12 lo 283 mg/ft3 and In furniture from 57 to 1,100 mg/fr, only 14-30% of lead was removed from cerpets; 5 40% from furniture. 500 pg/g (leed/lotal dust) action level for cleanup advisory. Lead mining and melting Work practice! questionnaire. Sample* of floor dust, window till dull, paint and tap water were analyzed for lead. Lead in window sill dust 30-27,900 ppm, floor dust 8-11,000 ppm. Positive association between miner wearing work clothes home and BLLs In children. Varfoui lead Induifrlei Telephone Interviewer* liked about ahowerlng at work, wathlng clothe* at home, etc. The data Indicate that elevated blood lead levela In children ate asaoclaled with parent* washing dirty work clothing at home. Dili collected after June 1992. 187 Tible 17. (Continued) Federal Lm Relevant to Worteri' Home Contamination Popular Name PubIk Law Asbestos Haurd Emergency Response Act of 1986 Public Law 99-J19 Retklentlal Lead-Bsted Paint Hazard Reduction Act of 1991 PL 102-550 Title X Subtitle B U.S. Code (15 U.S.C | 2642 ft Seq.J (15 U.S.C : 2681 ft Seq.J Section* Relevant to Workers' family Protection 12646 Contractor and laboratory accreditation (b) Accreditation by State (1) Model plan (B) Plan requirement! (xl) Hauiekeepln| and persona! hygiene practice!, Including the nececelty of thowera, and procedure! to prevent asbestos exposure to an employee's family. f 2681 DeFinilioni For the purpose! of thii subchspter (I) Abatement The term "abatement* means any set of measure! designed to permanently eliminate leadbaied paint hazards In accordance with standard! established by the Administrator under this lubchapter. Such term Includes- (A)the removal of lead-based paint and lead-canlamlnaied dust, the permanent containment or encapsulation of lead-based paint, the replacement of lead-painted surfaces or fixtures, and the removal or covering of lead-contaminated soil; and (B) all preparation, cleanup, disposal, and poslabilement clearance testing sctlvltlei associated with such measures. (II) Lead-coni smln*led dust The term "lead-conttmlnited dust* means surface dust In residential dwellings that contains an area or mass concentmlion of lead in excess of levels determined by the Administrator under this subchspter to pose threat of advene health effects In pregnant women or young children. (12) Lead-contaminated soil the term *lead-coniamlnaled soil* means bare soil on residential real property thit contains lead at or In excess of the levels determined to be hszardous to human health by the Administrator under this subchspter. f 2683 Identification of dangerous levels of lead Within IB months after October 28,1992, the Administrator shall promulgate regulations which shall Identify, for purposes of this subchspter, and Ihe Residenlial Lead-Based Paint Haunt Reduction Act of 1992 [42 U.S.GA. ( 4851 et seq.], lead-based paint haurdi, lead-contaminated dust, and lead-contaminated soil. 221 RUI-E/CTR NO. Inorganic arsenic [29 CFR 1910.1000] (general industry) (29 CFR 1913.1018] (shipyards) [29 CFR 1926.1118) (construction) Adbcatoa [29 CFR 1910.1001] (general industry) |29 CFR 1913.1001] (shipyards) |29 CFR 1926.11011 (construction) Cadmium [29 CFR 1910.1027) (general induitry) [29 CFR 1913.1027] (shipyards) (29 CFR 1926.1127] (con struct ion) Hazard Communication (29 CFR 1910.1200] (general industry) (29 CFR 1913.1200| (shipyards) (29 CFR 1926.591 (construction) Hazardous Waste Operations and Emergency Recpotue [29 CFR 1910.120] (general industry) [29 CFR 1926.65] (construction) Table tH. Riptilioru of Pcdcnl Agencies Relevant to Workers' Family Protection AGENCY OS1IA DESCRimON OF RRUIVAhTF ELEMENTS The PBL Is 10 as an H-hr. average. Where employees work in areas where exposure concentrations exceed I0^ig/m^ or where the possibility of skin or eye irritation from inorganic arsenic exists, the employer must provide clean protective work clothing weekly (daily if exposure levels exceed 100 Ml/m'*). Protective clothing must be removed in change room* and placed In a closed container prior to removal for cleaning, laundering or disposal. The container must be labeled and the Uundentr informed of (he hazards. When exposures exceed 10 the employer must provide showtrt and separate storage facilities for street and work clothes. OSHA PEL is 0.1 fiber/ce as an 8-hr, average. Excursion Umit (EL) is 1 fil>er/ec as a 30-min. average. Where employees are txposed above these limits, or where the possibility of eye irritation exists, the employer must provide, and ensure: that the employee wears appropriate protective work clothing; that contaminated clothing is removed only in change rooms; that no employee lakes contaminated work clothing out of the change room (except those authorized la do so for purposes of laundry, maintenance and disposal); that containers for contaminated clothing are labeled; that laundering is done in a way Ihat will minimize release of fibers to the air; that the Inunderer be informed of the hazards; and that contaminated clothing be transported in sealed containers. The employer must provide facilities to assure that street clothes do not become contaminated If the employeea' exposures exceed the PEL, that such employees shower at Ihe end of the work shift and that they do not leave the workplace with any clothing or equipment worn during ihe work shift. OSI1A In addition to the requirements for general industry, clothes of workers who work In certain regulated areas where the decontamination area and the shower cannot be located next to the regu[ated area, must be vacuumed with a HEPA vacuum cleaner before proceeding to the shower, or the employee must remove contaminated clothing in the equipment room and don clean work suilt before proceeding to the shower. For other regulated areas, work clothing must be vacuumed before il Is removed, but showering Is not required. A The PEL is 5 Mg/mJ as an 8-hr. average. If an employee is exposed above the POL or where skin or eye irritation is associated with cadmium at any level, ihe employer must provide clothing and equipment that prevents contamination or the employee and the employee's garments. Contaminated clothing must be removed at the end of the work shift In change rooms which have separate storage fadlilies for street clothes and work clothes. The facilities must be designed to prevent contamination of the street clothes. The employer must assure Ihat employees exposed above the PEL shower during the end of the work shift. The employer must assure that no employee takes contaminated protective clothing from the workplace, except when authorized to do so for laundry, cleaning, maintenance or disposal at an appropriate location or facility. Contaminated clothing must be stored In a closed container, and labeled. Launderen and cleaners must be informed of hazards. OSHA These standards have elements that could be used for preventing workers' home contamination. These elements include; the written hazard communication which employers must prepare; the requirements that all containers or hazardous chemicals be labeled; the requirement Tor preparation of material safety data sheets containing Information on applicable precautions for cafe handling and use, Including appropriate hygiene practices, work practices, or personal protective equipment; the requirement for employee information and training. OSHA These standards require l written safety and health program Tor employees involved In hazardous waste operations. Among Ihe requirements are: use of appropriate protective equipment for each hazardous waste site; appropriate decontamination of alt employees and contaminated clothing and equipment before leaving the area; location of Ihe decontamination procedures to minimize cross-contamination; removal of protective clothing or equipment from the site only by authorized employees; advising laundries and cleaning establishments of the hazards of contaminated clothing; and provision of showers and change rooms outside of the contaminated area, when the need Is indicated. 237