Document Gg6BYxpNvemmY1GDkJgYZRZx

/ \ y\ TESTIMONY OF RICHARD LEWIS OCCUPATIONAL HEALTH SPECIALIST INTERNATIONAL CHEMICAL WORKERS UNION BEFORE THE SUBCOMMITTEE ON HEALTH AND SAFETY OF THE HOUSE SUBCOMMITTEE ON EDUCATION AND LABOR ON THE WORKER'S RIGHT TO KNOW AND THE WITHDRAWAL OF OSHA'S PROPOSED RULE ON HAZARDS IDENTIFICATION July 14, 1981 Washington, D. C. S,U 000060913 CONTENTS Introduction i. what the worker needs to know 1. Chemical Identity 2. Hazard Notification ^, 'r.fl II. USE OF RIGHT TO KNOW INFORMATION III. COMMENTS ON CMA TESTIMONY 1. Chemical Industry Safety Record 2. Overlabeling a - 3. The ANSI Standard 4. General vs. Workplace Specific Hazard Determinations 5. Are-Chronic Hazard Determinations Beyond The Present State Of Science 6. Mislabeling 7. OSHA Rulemaking Procedures CONCLUSION REFERENCES APPENDIX SAL 000060914 1- - INTRODUCTION Mr, Chairman, my name is Richard Lewis. I am an occupational health specialist on the staff of the International Chemical Workers Union (ICWU). First,let me say ICWU greatly appreciates the opportunity to talk to you about efforts to reverse the pattern of occupational illness and injury in American workplaces. Public health, working in cooperation with government*has a proud tradition in this country of eradicating wide spread disease. The track record has been brilliant in the area of infectious disease such as polio and measles. Unfortunately, the same type of progress has not yet been made in the area of occupational injury and illness. Data from the Bureau of Labor Statistics "Occupa tional Illness and Injury in U.S. Industry," indicates a total of 36,178 lost workday cases resulting in over.half a million lost workdays in the Chemical and Allied Products Industry alone."' I want to emphasize these numbers are only for one year. We are talking about 4 1/2 to 5 million lost workdays due to injury and illness in the last decade in the Chemical and Allied Products Industry alone. No attempt has been made to quantify the ripple effect as chemicals move from manufacturers to downstream users, but the National Occupational Hazards Survey (NOHS) p indicated that potential hazards exist downstream as well. This represents a monumental problem from a public health point of view and obviously a tremendous amount of pain and suffering for workers. SAL 00006091s 2- - Fighting for the prevention of.occupational injury and illness has been a long hard struggle for public health advocates and workers. In the last ten years, under both Democratic and Republican administrations, the federal government has initiated a variety of programs under the Occupa tional Safety and Health Act aimed at the prevention of occupational illness and injury. Some of the most important programs ^include health "K. standards regulating carcinogens and access to medical records, the New Directions program, and a policy favoring engineering controls over personal protective equipment as a means of worker protection. These tools for health and safety protection are a desperately needed beginning. ilCWU believes that identification of chemicals and hazard notification is a crucial next step in the development of a comprehensive health and safety program. Unfortunately, chemicals continue to directly threaten the well-being of workers with discouraging regularity by exploding, igniting, producing acid and alkali burns, intoxicating and suffocating workers in enclosed spaces, and producing long term chronic hazards such as cancer. The Right to Know for the worker boils down to "what is it?" and ,lwhat will it do to me?" In presentation of this testimony, ICWU decided it would be useful to demonstrate that workers are unable to obtain the needed information to determine the identity and hazards of the substances they are exposed to each day. We have done this in Section I of our testimony which relies on examples from our files to demonstrate this inadequate flow of health 000060916 3- - SAL t and safety information to workers. However,it should be noted that I will cite only a few examples. I can tell you that we do not have a single local in which workers are fully advised of the identity and hazards of their exposures. Section II of the testimony will demonstrate that workers are motivated and able to work with health and safety information and data when they are able to obtain it through requests to the company, NIOSH, OSHA, or the National Labor Relations Act. ^ In Section III of the testimony we will specifically respond to the Chemical Manufacturers Association (CMA) testimony given to this Sub committee on May 27, 1981, and point out where that testimony contradicts scientific principles of occupational safety and health and indicate our experience at the local plant level. .1 will turn now to the first major section of our testimony which describes what kind of information the worker needs to know. I. WHAT THE WORKER NEEDS TO KNOW 1. Chemical Identity The two questions:"what is it?" and "what will it do to me?" are interdependent. If a worker, an industrial hygienist, or a doctor does not know the identity of a substance, there is hardly any way he or she can determine what health risk may result from exposure. A worker can not take the simple step of referring to a toxicology text which many ICWU SAL 000060917 4- - locals now have in their libraries. A doctor, when presented with an ill worker, can not properly diagnose or treat an illness unless knowledge of the illness causing agent is readily available. One certain way to make the information readily available is to indicate the chemical identity and hazard of the chemical on the label. The ICWU health and safety staff receives "what is it?" requests from workers on a weekly basis. The following examples are-excerpted from the full text of letters in the ICWU health and safety files. No one in the plant knows what it is.. The customer sent everything pre-measured and in the code of 001-005. How do I go about getting chemicals in the product? The local member in this example is referring to the names of various chemicals in the product. The worker needs these names to see if the product is hazardous so that safe work controls can be utilized. Four members have been complaining of"a rash on their arms and bodies. One member has been getting sick while in : - contact with this dust. The odor of this machine smells like a dead animal. I have asked the company on May 8 for a material status and manufacture name, but to date haven't received any thing. Any information as soon as possible will be appreciated. We are going to start the line up today; 5-19-81. This is a case of workers experiencing potentially occupational induced symptoms, yet all they know, about the exposure is that barrels are marked "150#." " Many labels presently in use do not identify the chemicals present in the product. For example the health and safety staff received a letter 5- - i' sal 0000609 1 requesting specific health information on paint. As you can see by looking at the label in Appendix A-l, the specific chemical ingredients of the paint are not given; instead, broad categories of chemicals are listed. The use of a broad category such as aliphatic solvent presents both a safety and a health hazard. A safety hazard is present in that workers .are unable to determine the flash point and consequentli|brevent a potential explosion resulting from use in an enclosed spice. A health hazard is also present. A category or class of chemicals contains individual chemicals which, range from very'toxic to relatively nontoxic. A worker who only knows he or she is exposed to aliphatic ov solvents can't tell .if.the exposure is to ethyl acetate, which may cause 3 some irritation to the nose and throat, or to xylene which causes irri tation but at higher levels of concentration has caused dizziness and even .death.4 Please note Appendix A-2 for the list of some twenty chemicals used as solvents, in paints. Use of some of these solvents require stringent ventilation controls, others do not. This paint label does little to provide the health and safety information needed for adequate protection when exposure to toxic ingredients may be present. ICWU has recent examples in their health and safety files of cases where workers have been exposed to known or suspect carcinogens that they were unable to identify. 4,4`-Methylenebvs (2-Chloroaniline), commonly referred to as MOCA, is a curing agent used in epoxy resin systems. ICWU workers were exposed to MOCA in a nozzle cleaning operation in a Gulf And Western plant. V-: SAL 000060919 -6- The carcinogenicity of MOCA is well established. The American Conference of Government Industrial Hygienists stated the following in 1976. Based on animal experiment, Cl.-MDA (MOCA) is suspected of carcinogenic potential in man; worker exposure by all routes should be carefully controlled.^ In 1978 NIOSH published a Special Hazard Review on MOCA which included this statement in its conclusion. Results reported by five independent groups of investi gators clearly demonstrate 4-4' Methylenebis (2-Chloroanaline), to be oncogenic (tumor forming) in the rat, mouse, and dog. Ingestion of daily doses of 4-4' Methylenebis (2-Chloroanaline) by mice and rats have resulted in the appearance of cancer of the liver, kidney, lungs, skin, and mammary glands. Reports of cancer findings on MOCA are also documented in the 1975 edition of Occupational Medicine, a well respected text by Dr. Carl Zenz. Although industrial experience from reported studies is minimal, the positive findings in two animal studies by three independent investigators firmly implicate 4-4'-Methylenebis (2-Chloroanaline) as a human card nogen. 7 MOCA is readily absorbed through the skin; therefore prevention of skin contact exposure to MOCA is an essential industrial hygiene control measure. Workers would vigorously adhere to protective measures if they knew exposure to a carcinogen was involved. In the early 1970`s NIOSH estimated 55,000 U.S. workers were o potentially exposed to MOCA. OSHA attempted to regulate MOCA along with 13 other carcinogens in 1973, but the final MOCA standard was remanded for procedural reasons by the Court of Appeals, 'Third Circuit 7- - ,0920 00006 B&L- f i (Synthetic Organic Chemical Manufacturers Association v. Brennan 506 506 F2d 385, 1974). However, various states such as California continued to enforce the standard under State law. The experience at the ICWU local was that workers were not notified of their exposure to MOCA. The company denied that MOCA exposure existed in the plant, yet MOCA appeared in a urine sample^^ an exposed worker and in an OSHA industrial hygiene sample of the nozzle cleaning solution. In this case exposure to a known carcinogen was taking place. The carcinogenic properties of MOCA have been described in a number of well accepted and widely used occupational health references. There is no excuse to keep workers in the dark about the presence of MOCA in the plant nor about MOCA being a suspect human carcinogen. ICWU has embarked on a major hazard notification computer program with the cooperation of NIOSH. Ideally,the computer program would be used to immediately notify exposed locals as soon as the scientific hazard information becomes available. However, the system is dependent on proper identification of the materials used in plants. When ICWU locals request lists of chemicals used by a company, they often receive useless trade name information. A very recent ICWU example of exposure to acrylonitrile demonstrates that the use of trade names constitutes a road block to the meaningful flow of health and safety information to workers. Acrylonitrile is a metabolic q asphyxiant with an action similar to cyanide, but perhaps more serious because more frequent is the epidemiological evidence that^shows that low level exposures may be associated with an excess of lung and colon cancer in workers.^ -8- SAL 000060921 Workers at this local were only informed of the cancer causing properties of acrylonitrile when the local president had occasion to read an ICWU hazard alert during a labor management meeting. The alert included a list of acrylonitrile trade names,one of which a worker recognized as being present on a label in the plant. The ICWU hazard alert came out in 1981, A NIOSH Current Intelligence Bulletin pub! ished-.information on excess human cancer rates in acrylonitrile workers in 1977.^ The example of employees being exposed to trade name products containing carcinogens is fairly widespread according to the NOHS survey undertaken by NIOSH in 1972. The survey found that, of workers using trade name products (TRN) in the course of their employment, some 2% (5,638 workers) were potentially exposed to one of the fifteen chemicals that OSHA regulated as carcinogens. OSHA has regulated only a small fraction of the chemicals currently documented as having substantial evidence of .carcinogenicity; so the 2% figure is below the actual figure for workers potentially exposed to trade name products containing carcinogens. The previous set of examples demonstrate that workers exposed to hazardous substances are often unable to answer the basic question, "what is it?" 2. Hazard Notification Once the identity of the chemical can be established the worker is still not in a position to assess the health and safety implications of a situation. To determine what the hazards are the worker must now turn to his or her own occupational health information resources, the union SAL 00006092 9- - health and safety department if the workers belong to a union, or the company. The following are examples of information requests from locals where the chemical identity was known but hazard information was not known. Examples are excerpted from the full text of letters appearing in the ICWU health and safety files. Workers often ask questions about specific control methods for hazardous chemicals. When there is suspect exposure above TLV should there be follow examination by the medical department? Question #4 - Has Thiotepa been determined to cause cancer in animals? Question #5 - What precautions has the company taken to protect its employees? The now withdrawn OSHA labeling standard offered a reasonable and scientifically valid approach to the hazard determination process. The process attempted to set objective scientific criteria for hazard determi nation which are commonly used in the field of public health. Such a hazard determination process would insure a comprehensive set of hazard evaluations would be passed on to workers. A performance oriented approach, such as the one suggested by the CMA Guidelines in Exhibit 1. of their May 27 testimony, could result in as many different evaluation results *as there are manufacturers to do the evaluating. ICWU workers are being provided with inadequate hazard information by their employers. ICWU workers were notified by Lederle Laboratories of American Cyanamid in early 1978 that it was unsafe forewomen of child -10- SAL 000060923 vll- bearing age to be exposed to two drugs that were being manufactured in the plant: methotrexate and diamox. The company instituted a policy barring women of '"childbearing potential" from certain sections of the .plant. In December of 1978 the company communicated to the union that they had determined a safe level of exposure for women of "childbearing potential" to methotrexate and that women would no longeriSe'restricted j 4 ; from diamox production. The Physician's Desk Reference text used by doctors in prescribing drugs* links methotrexate wittya reproductive disorder in males,This information was Kcr'f' communicated by American Cyanamid to their workers Owoh'* ikvolv'cwiifl\ A more widespread ^example of. inadequate, hazard, evaluation and notification pertains to the chemical Toulene - 2,4-Diisocyanate. A NIOSH study conducted in 1972-1974 estimated that 50,000-100,000 U.S. workers were potentially exposed to Diisocyanates. 15 TDI exposures in a number of adverse health effects one of which, sensitization, > is particularly disabling. Sensitization to TDI denotes the tendency of some individuals to suffer a progressively more severe respiratory reaction when exposed to very low levels. Although the acute effects may be severe, their importance is overshadowed by respiratory sensitization in susceptible individuals; this has occurred after repeated exposure to levels of TDI as low as 0.02 ppm and below. The onset of symptoms of sensitization may be insidious, becoming progressively more pronounced with continued exposure over a period of days to months; initial symptoms are often nocturnal dyspnea and/or nocturnal cough with progression to asthmatic bronchitis. Often when the respi ratory illness has become incapacitating and 0000&0924 SAU 11- the worker has been hospitalized or otherwise removed from the worksite, a return to work causes an acute and severe asthmatic attack almost immediately or within a few hours.16 A sensitized worker may never be able to return to his or her work place or any other workplace where TDI is present. Although the sensitization effects of TDI are documented in medical textsstudies 1O published in the American Industrial Hygiene Journal, slid NIOSH documents, sensitization warnings do not presently appear on labels of TDI used in a foaming operation of an ICWU shop. Because TDI can cause serious damage at extremely low levels it is important that yet unsensitized workers be aware of potential hazardous exposures so to avoid sensitization. More dramatically it is critical that sensitized workers are properly informed of TDI and its hazards so they can avoid debilitating acute respiratory reactions. In summary,these previous examples demonstrate that workers are un able to obtain important information about what they are working with and what it can do to them. Examples are cited of how identification of trade name is not a useful health and safety practice and how a performance oriented hazard evaluation scheme fails to supply meaningful and accurate health and safety information. These examples stress that workers need both chemical identity and hazard information to protect themselves. ICWU wishes to emphasize that what public health advocates and workers want from a Right to Know standard is that labels and material safety data sheets reflect available scientific information. It makes little sense to ICWU to fund projects on the hazards of chemicals, e.g., the National Cancer Institute 12- - SAL 000060925 Genetox study, and then fail to inform those who must work with these chemicals of findings of adverse effects. II. USE OF RIGHT TO KNOW INFORMATION There are several disciplines of public health professionals including occupational physicians, industrial hygienists, and epidemiologists who 'rgi'' would be better able to practice if hazardous workplace chemicals were properly identified. This testimony has mentioned previously the dif ficulties that the ICWU health and safety staff has in carrying out hazard alert notification when we cannot determine what exposures workers are experiencing. I am sure this committee will hear the testimony of public health scientists outlining the importance of obtaining exposure information, but we are here today to speak mainly for workers' need of Right to Know. Although workers in ICWU locals receive professional support from the international, we serve 60,000 workers and have a limited health and safety staff. No union in America can fully service the health and safety needs of all its members. Much of the research must be done by members at the local level. ICWU has trained some 800 local leaders in hazard recognition and other health and safety practices over the last two years. Proper identification of chemicals would greatly enhance the ability of these workers to fully put this training to use. A Right to Know standard* * Epidemiology is the science of examining the occurrence of disease in populations. -13- SAL 000060926 -is even more essential to the approximately 75 million unorganized workers in this country who do not have a professional health and safety staff to turn to for assistance. ICWU experience has shown that local members are highly motivated and able to collect occupational health information on the problems that occur in their shops as the following examples demonstrate. The reason for this letter is to open an avenue for questions concerning the health and well being of our people. Being new at this positional am quite ignorant of the short and long term effects of many chemicals we work with regularly and am in need of any material available on the subject. Two chemicals I particularly want information on are Phosphorous Oxychloride and Ethylene Dichloride (EDC). I understand that there has been a change in status on EDC and would appreciate any update on this. Also, 1 have been personally affected by Phos. Oxy. in the past, yet in the few books I have on chemicals, I can find no reference to effects of this chemical nor any threshold limits. In short, just how harmful are these two. Last duly I asked (name deleted) for some information on the Thiotepa that is manufactured in Department #721. At that time I asked (name deleted) how long were they going to run Thiotepa? He was not sure and would get back to me. Can you answer that question. How long does Thiotepa **un take and how many times a year do we run Thiotepa? Question #2 - Are you monitoring for exposure levels? What are those levels? Question #3 - Does Thiotepa cause any toxic effects on the body? If it does what are they? Question #4 - Has Thiotepa been determined to cause cancer in animals? Question #5 - What precautions has the company taken to protect its employees? I would appreciate your answer as soon as possible. When we receive your answers we may at that time have additional question to ask. -14- sal 000060927 In a few cases ICWU locals have gone several steps beyond basic hazard identification and carried out crude epidemiological surveys. For example, members of one local did the initial data collection on the association between exposure to the pesticide oryzalin and birth defects in exposed workers. This information sparked the interest of the New York State Health Department, NIOSH, and OSHA, who are still involved in the process of investigations. Members of another local carried out a crude epidemiological survey. Eventually, with the help of a local independent occupational health expert from the Philadelphia Area Project on Occupational Safety and Health, the local determined that exposure to fluoride dust could be associated with the occurrence of illness in the plant. v. ...First of all I went through the pink slips, I placed them on the jobs, how long they worked in the drying room, when they got out and what reasons they got out for. Some of the employees I talked to had holes in their septum, bleeding noses, eye irritations, sore noses and many other symptoms. I took a few symptoms I know of to start with and left each employee as I talked to him, tell me how they felt when they worked in the drying room. This way if something was mentioned that another one had said to me I asked him if he felt this symptom and most of them added more to it. Starting out with five symptoms, I ended up with 17 different symptoms from perforated septums to one employee who had no problems but only worked in the area a short period of time. Although the determination, persistance, and assessment skills of these workers prevailed in the above examples, we don't see any reason why there should be so many obstacles and barriers between workers and health hazard information. Most manufacturers know the health hazard information on the chemicals they produce and they should be made to share such information. Health -15- SAL 000060928 hazard data must not be treated as trade secret information. Union health and safety professionals and workers should not have to ferret out health hazard information that is already known. III. COMMENTS ON CMA TESTIMONY The ICWU health and safety staff has had the opportunity to read the testimony offered by representatives of the Chemical Manufacturers Association to this Subcommittee. We will comment on that testimony at this time. 1. Chemical Industry Safety Record The CMA testified that the chemical industry is the second safest industry in America according to National Safety Council Data. 1 9 This relative ranking should not obscure the magnitude of the health and safety problem in the chemical industry as documented by the Bureau of Labor Statistics. The record of health and safety in the chemical industry clearly demon strates that worker health is endangered. According to Bureau of Labor Statistics the rate of workplace injuries and illnesses in the Chemical and Allied Products Industry was 7.8 per 100 workers in 1978. 20 This figure represents a decrease of reported injuries and illnesses over the previous six years. The category of lost workday cases represents a subset of ill nesses and injuries that are more serious than the previous category. The 1978 rate was 3.3 lost workday cases per 100 workers. This rate has increased over the past six years. Although the rate of injury and illness is decreasing slightly, the rate for the more serious injury and illness category is increasing slightly. -1 6- SAL 000060929 ICWU suspects that the lost workday cases reflect the more chronic illness and injuries in the workplace. A Right to Know standard must deal with chronic hazards to be effective in reducing workplace disease. As mentioned earlier in this testimony, over one-half million workdays were lost in the Chemical and Allied Products Industry due to occupational injury and illness in 1978 alone. These statistics in their present form show that there are serious health and safety problems in the chemical industry. However, there is reason to believe that these statistics are underestimates due to the inability of the reporting service to continuously pick up workers who have left work due to chronic illness and have not returned. There is also reason to believe that under-reporting of occupational illness does exist as a result of a lack of recognition of occupationally-related illness by doctors and members of society in general.22 An Interim Report To Congress On Occupational Diseases published in 1980 cited data indicating the magnitude of the lack of recognition of occupational disease. This survey suggests that of 1.8 million disability awards under state workers' compensation programs in 1978, approximately 30,000 or only 1.7 percent were for occupational diseases." We would like to call to the attention of the Subcommittee a recently released report entitled Occupational Safety and Health in the Chemical Industry issued by the Council on Economic Priorities (CEP). The report concluded that the severity of 0SHA violations in the chemical industry "exceeds all other U.S. industries except mining."24 The Council on Economic Priorities used records of 0SHA inspections, citations, and -17- SAL 000060930 violations to measure the safety of industries. Evaluation of health and safety is a difficult exercise but the study clearly addresses health hazards in the industry. 2. Overlabeling As we have demonstrated with numerous examples, proper chemical identification and hazard notification is far from the rule in ICWU shops. Our experience has shown us that many employers do not provide this information nor do they show respect for the worker's desire to obtain information on his or her daily exposures. The CMA testimony contained references to their concern for "overlabeling" of workplace substances. Excessive, unwarranted hazard warnings would dull the awareness of workers for hazard communications that are soundly based.25 ICWU disagrees with this assessment and is confused as to why the CMA is speaking for workers in this instance. Workers are more concerned about benzene and other neurotoxic solvents dulling their senses than hazard warnings dulling their senses. As to the technical complexity of the withdrawn standard, ICWU appreciates that some scientific information is difficult to understand. In addition, ICWU appreciates that large numbers of substances may require labeling as a result of a scientific evaluation process. However, public health and medical scientists have a long tradition of collecting, analyzing, and interpreting health hazard information and they have arrived at a workable consensus on the scientific principles that govern the process. Neither complexity nor the frequency of potential labeling justifies ignoring any valid scientific information. SAL 000060931 -18- 3. The ANSI Standard In regard to the CMA claim that the American National Standards Institute Standard for Precautionary Labeling of Hazardous Industrial Chemicals (hereinoc after ANSI Standard) has been used effectively by the industry, we disagree. The ANSI Standard is woefully inefficient in its approach to chronic health hazards as noted by the Committee on Government Operations 1976 report. Voluntary labeling guidelines developed by the chemical manufacturing industry are directed primarily tdvthe avoidance of injury from single, accidental exposure and do not address the health hazards caused by chronic low-level exposure to toxic chemical substances/' Moreover, the NOHS survey clearly suggests that the industry is not following its own recommendations in notifying downstream users of hazardous oo chemicals. 4. General vs. Workplace Specific Hazard Determinations CMA makes the argument that some chemicals with known hazardous effects need not be labeled as hazardous because actual foreseeable plant handling and use present no adverse health risk. Our experience in industrial hygiene suggests this is not the prudent course. For example, it is expected that a worker running a chemical process through an enclosed system will not receive exposure. However, what if the system develops a slow leak or some other emergency arises? This is a situation in which hazard identification is needed. The normal foreseeable process sometimes breaks down. That is what accidents and emergencies are all about. Accidents involving toxic chemicals are life threatening and we believe workers should have the information to be prepared in the case of an accident. We know from practical experience that some workers tend not to push for ventilation or equipment repair or even report malfunctioning equipment -19- SAL 000060932 becauseof job production pressures. All exposed workers should be aware of the potential consequences of such neglect. The ICWU health and safety staff also rejects any contention that some hazardous substances should not be labeled as hazardous because they appear in a nonhazardous form. Public health protection calls for the labeling of any hazardous substance in all its forms, because physical states of substances often change intentionally or unintentionally in chemical production and use. An illustration of this change of physical state is the case of a hazardous powder that is shipped in a block form and therefore assumed to be safe. However, the substance in the block form may be worn down at the edges to powder by handling or may be crushed in a later manufacturing state. A chemical producer does not and cannot know all of the downstream uses of a product, therefore, the prudent public health course is to label a known hazardous substance in all its forms so workers in all plants and in all manufacturing processes will be informed of potential hazards. 5. Are Chronic Hazard Determinations Beyond The Present State of Science? CMA contends that OSHA's now withdrawn hazard identification scheme is beyond the present state of science^ and outside of the area of scientific consensus.^ CMA cited the inability of the present state of science to develop an objective definition of a reproductive hazard.^ However, epidemiologists and clinicians routinely conduct studies and publish con clusions that determine the reproductive hazard of a substance. Modern occupational medicine texts contain such information. For example, 1,2 Dibromo-3-chloropropane (DBCP) is described as follows in the Proctor and Hughes text. -20- SAL 000060933 DBCP causes sterility in male workers and cancer in mice and rats... DBCP has caused oligospermia (scarcity of spermatozoa in se^en) and aspermia (nonemission of semen) in male workers. 3 Anesthetic gases such as halothane and ethrane which are used to put people to sleep in hospital operating rooms have been shown to be a reproductive hazard in workers and experimental animals. A 1973 study of female nurse-anesthetists in Michigan found a three fold excess of birth defects in mothers who continued to work in operating rooms during pregnancy compared to those who left the operating room during that period.^ A NIOSH study of operating room personnel revealed an increased risk of miscarriage for women employed in operating rooms compared to nonoperating room employees. 35 Results from animal studies indicate the reproductive hazards of halothane. Basford and Fink (1968) reported that when rats were exposed to 0.8 percent halothane for 24 hours on day 9 a significant increase in defects of the ribs and vertebrae were found in the offspring as compared to co^rols exposed to air and also starved during day This is the sort of "objectively ascertainable end results in humans or other mammals" 37 information that the withdrawn standard called for to undergo examination by the criteria for a reproductive hazard. Since physicians routinely treat patients for chemically induced reproductive disorders and scientists are studying reproductive disorders, why can't workers be informed of their scientific conclusions? 6. Mislabeling CMA also makes various claims that the evaluation scheme under the now withdrawn standard would have lead to mislabeling and labeling substances as carcinogenic based on "allegations" of carcinogenicity. These claims cannot be supported. -21- SAL OOO06Q934 For example there is no support for the following claim. These statements from OSHA lead to the conclusion that, under the now-withdrawn proposal, almost any allegation of carcinogenicity for a substance would have required its being labeled as a carcinogen.38 Under the withdrawn standard, the determination of a health hazard can only be made through a series of evaluative steps common in scientific practice. None of these steps give any credibility to "allegations." These steps are published in Appendix B of the withdrawn standard on pages 4450 and 4451 of the January 16, 1981 Federal Register. These evaluative steps acknowledge the scientific credibility of well controlled scientific studies, statistically significant conclusions, case reports, expert opinion, and peer review journals. The withdrawn standard actually states on page 4434 that information of any lesser quality will not be utilized in hazard evaluation. The evaluation procedure does not-consider anecdotal material because the Agency does not believe that such "data" warrant a positive hazard determination under this standard.(Emphasis .added) A second example of an incorrect CMA claim concerns the following CMA statement: OSHA's specification proposal for determination of chronic hazards would have resulted in much mislabeling. For example, OSHA's proposal would have required inap propriate labeling as carcinogens of materials such as acetic acid (vinegar); boric acid (eyewash); fructose, lactose and maltose (natural sugars); and sodium chloride (table salt). These materials are so designated in the NI OSH Registry of Toxic Effects of Chemical Substances. (RTECS7)"TM It is true that NIOSH RTECS must be consulted in the process of the required literature search as stated in Appendix A of the withdrawn standard. However, it is not true that the evaluator is bound to accept a -22- SAL 00006093 hazard description because it appears in the NIOSH RTECS. The hazard determination scheme for any health hazard, including cancer, is laid out in a series of evaluative steps in Appendix B on pages 4450 and 4451 as previously noted. RTECS will only serve as a starting point to inform the hazard evaluator what studies must be consulted. RTECS is listed under the category "Materials To Be Reviewed." Once these material%are identified the evaluator must follow the scheme set out in Appendix B, a scheme which lists scientific criteria and does not necessarily accept judge mental statements that appear in studies in RTECS. In review, chemical identification and hazard notification can be derived from sound industrial medical science. We reject the notion that such utilization of scientific information is beyond the present state of science. The ICWU health and safety staff confers with scientists and physicians on a weekly basis who use such terminology as reproductive hazard and carcinogen as the tools of their trade. 7. OSHA Rulemaking Proceedings ICWU is concerned about future OSHA proceedings on the Right to Know. Dr. Smith of the CMA expressed a preference for OSHA to pursue "open, smaller, less-formal meetings," 41 as opposed to formal OSHA public hear ings mandated by the Administrative Procedures Act (APA). ICWU is not sure what an "open, smaller, less formal meeting" is, but we emphatically encourage OSHA to utilize APA rulemaking procedures if they are interested in developing a rulemaking record that reflects the interests of all affected parties. -23- SAL 000060936 CONCLUSION We hope this information will be useful to the Subcommittee in evaluating the Right to Know. Basically we are here tody to state that workers should have access to health effects information that has been generated by various fields of public health science. In closing, I would like to recount to you a set of events that transpired last summer in an ICWU local shop of a Conoco plant in Baltimore. The scientific and political arguments about Right to Know should never be viewed outside the context of the day to day health and safety danger that workers face. I opened this testimony by quoting a set of cold and impersonal government statistics, but will close with a different view of the problem. Mark Edmunds, an employee of the Baltimore Conoco plant, is a member of ICWU. Early last summer Edmunds was assigned to clean a chemical tank that contained benzene residue. He refused the job because he believed it to be too dangerous. On the morning of August 6, 1980, four day workers were hired to clean the chemical tank that contained the benzene residue. After a few hours work the men were leaving the tank for a second break from the harsh fumes. At this moment one worker, Linwood Bryant, age 40, fell unconscious to the floor of the chemical tank. Bryant was taken from the tank. Conoco lab technicians attempted to revive him. Linwood Bryant was pronounced dead at 2;45 p.m. that same afternoon. An autopsy confirmed that Bryant died of acute benzene poisoning. SAL 00006093? -24- I hope this one small example42 demonstrates the seriousness of risks that workers are unknowingly exposed to in American workplaces. I would be happy to answer any questions at this time. -25- SAL 000060938 REFERENCE5 1 . Occupational Injuries and Illnesses in the United States by Industry, 1978, U.S. Department of Labor, Bureau of Labor Statistics, Washington, August 1980, p. 29. (Hereinafter cited as 1978 BLS Statistics.) 2. "Hazards Identification; Notice of Proposed Rulemaking and Public Hearings," Occupational Safety and Health Administration, Federal Register, January 16, 1981, p. 4415. (Hereinafter cited as OSHA Proposed Hazards Identification Rule.) 3. N. H. Proctor and U. P. Hughes, Chemical Hazards of the Workplace, 0. B. Lippincott Company, Philadelphia, 1978, p. 247. (Hereinafter cited as Proctor and Hughes.) 4. Proctor and Hughes, supra, p. 509. 5. A.C.G.I.H.: 4,41 -Methyl ene bis (2-chloroanil ine)'. TLVs Threshold Limit Values for Chemical Substances and Physical Agents in the Workroom Environment with Intended Changes for 1976. p. 38. Cincinnati, 1976. 6. 4,4'^Methylene bis (2-Chloraniline) Special Hazard Review with Control Recommendations, NIOSH, 1978, p. 11. (Hereinafter cited as NIOSH MOCA Review) 7. C. Zenz, Occupational Medicine, Year Book Medical Publishers, Inc., 1975, p. 862. (Hereinafter cited as Occupational Medicine by Zenz.) 8. NIOSH MOCA Review, supra, p. 2. 9. Proctor and Hughes, p. 90. 10. Current Intelligence Bulletin 18: Acrylonitrile, NIOSH, 1977, p. 1. 11. Current Intelligence Bulletin 18: Acrylonitrile, NIOSH, 1977, p. 1. 12. OSHA Proposed Hazards Identification Rule, supra, p. 4416. 13. See Appendix B for EPA Carcinogen Assessment Group List of Chemicals Having Substantial Evidence of Carcinogenicity. 14. Physicians' Desk Reference, Medical Economics Company, Oradell, N.J., 1980, p. 984. See Appendix C. 15. Occupational Exposure To Diisocyanates, NIOSH, 1978, p. 18. 16. Proctor and Hughes, supra, p. 483. 1,7. Proctor and Hughes and Zenz Occupational Medicine, supra. 18. Elkins, H.B. et al : Massachusetts experience with toluene di-isocyanate. Am. Ind. Hyg. Assoc. J. 23:265, 1962. Hygienic Guide Series: Toluene diisocyanate. Am. Ind. Hyg. Assoc. J. 28:90, 1967. -26- SAL 000060939 19. "Statement of the Chemical Manufacturers Association for the Health and Safety Subcommittee of the House Education and Labor Committee Hearing on the Withdrawal of the Department of Labor's Proposed Standard on Hazards Identification," May 27, 1981, p. 3. (Hereinafter cited as CKA Statement.) 20. 1978 BLS Statistics, supra, p. 29. 21 . 1978 BLS Statistics, supra, p. 29. 22. OSHA Proposed Hazards Identification Rule, supra, p. 4413, (statement of Dr. Thomas Mancuso). 23. Analysis done by ASPER, derivent from Hunt, A. Estimates of Compensated Occupational Disease Cases by Disease Type and Level of Disability, 1975 (unpublished) October 1977. 24. Occupational Safety and Health in the Chemical Industry, Council on Economic Priorities, New York City, 1981, p. 8. "Chemical companies are among the most hazardous; the severity of their violations exceeded those of all other U.S. industries with the exception of mining. In 1977 while all U.S. industry had 2.7 violations per inspection, the chemical industry had 7.7." 25. CMA Statement, supra, p. 7. 26. CMA Statement, supra, p. 2. 27. OSHA Proposed Hazards Identification Rule, supra, p. 4414. |28. OSHA Proposed Hazards Identification Rule, supra, p. 4415. &9. CMA Statement, supra, p. 5. 30. CMA Statement, supra, p. 6. 31 . CMA Statement, supra, p. 5. 32. CMA Statement, supra, p. 6. 33. Proctor and Hughes, supra, p. 202. 34. Corbett, T.H. et al . "Incidence of cancer among Michigan nurse anesthetists." Anesthesiology 38: 260-263, 1973. 35. Ad Hoc Committee on the Effect of Trace Anesthetics, American Society of Anesthesiologists, Occupational Disease Among Operating Room Personnel, Anesthesiology, Vol. 41, October 1974, p. 321-340. 36. Basford, A.B. and Fink, B.R.: The teratogenicity of halothane in the rat. Anesthesiology 29 : 1167-1173, 1968, from Catalog of Teratogenic Agents, T. Shepard, The Johns Hopkins University Press, Baltimore, 1980, p. 515. -27- SAL 000060940 37. OSHA Proposed Hazards Identification Rule, supra, p. 4429. 38. CMA Statement, supra, p. 12. 39. OSHA Proposed Hazards Identification Rule, supra, p. 4434. 40.. "Testimony By Dr. Curtis Smith On Behalf of the Chemical Manufacturers Association Before The Health and Safety Subcommittee On Education and Labor Concerning Hazards Communications," May 27, 1981, p. 4. (Hereinafter cited as Statement by Dr. Smith of CMA.) 41. Statement by Dr. Smith of CMA, supra, p. 7. 42. See Appendix D. for newspaper account and pictures. -28- SAL 000060941 SILVER-BRITE^ ALUMINUM PAINT -- B59 S 11 APPENDIX A-l >' SILVER-BRITE Aluminum Paint, B59 S 11, i is a ready mixed, general purpose aluminum [ paint for use on exterior and interior metal surfaces as well as masonry. SILVERBRITE Aluminum Paint can be applied by brush, roller or spray; however, roller appli cation produces the best results.- SURFACE PREPARATION: Surfaces to be painted must be clean, dry and free of oil, grease, rust and foreign mate rial. Prime exposed metal surfaces as soon as possible after cleaning. PRIMERS: Iron and Steel: Under 200F (93* C) KEM KROMIK METAL PRIMER, B50 N 2. 200 to 400F (93 to 204 C), apply directly to Near-White Blast cleaned surface, SSPCSP10-63T. Galvanized Iron: Galvanized Iron Primer, B50 A 1. Interior Masonry: Alkyd Wall Primer. Exterior Masonry (Concrete Block): block filler. Insulated Pipes & Duct Work: Latex Wail Primer. Previously Painted: Spot prime with the appropriate primer and follow with one or two coats of SILVER-BRITE Aluminum Paint. Application: Always apply to a cool surface. Do not shake with mechanical shaker or overly agitate. Follow recommended spreading rate '''osety. Allow first coat to dry overnight before applying second coat. CHARACTERISTICS CAUTIONS Contents are COMBUS REDUCTION: TIBLE. Keep away Iron Brush or Roller: Full body. heat and open flame Conventional Full body. May be USE ONLY WITH ADE Spray: reduced with up to 1 QUATE YENTH.ATIQII pint (.473 I) of Mineral Avoid breathing vapc Spirits, if needed. and spray mist. Avoi DeVilbiss JGA Gun, 78 contact with skin an or 704 Cap, FF Tip, eyes. Wash hands afte Airless Spray: Binks 18 or 19 Gun, 66 or 67 Cap, S Nozzle, 50 psi atomization pres sure, 20 psi fluid pres sure or equivalent equipment. RUBBERSET FLOMATIC G-10 Gun, Graco "Golden" Gun, .010-.012 orifice, using. Keep containe closed when not in ust- Do not transfer content to other containers ft storage. 0001 (9' DO NOT TAKE INTERNALLY KEEP OUT OF THE REACH OF CHILDREN Drying Time @ 77F (25 C) & 50% RH: Gloss: Coverage: 2,000 psi fluid pressure or equivalent equip ment. To touch: 1-4 hours To Recoat: 24 hours Bright Aluminum 690 sq. ft. per gallon (17 PROFESSIONAL. COATINGS SILVER-BRITE ALUMINUM PAINT Pigment By Weighl............. Aluminum Pasie Type 2 Class B ... 18% 16' Petroleum Resin . .. 19% Polymen2ed _ Linseed Oil......... ..21% ^SAliphaitc Solvent . .. 30% '"r Aromatic Solvent . .. 3% Additives............... . . 1% Heat Resistance: sq. m per I) @ 2.3 mils wet, 1.0 mil dry. Up to 400F (204 C). 4'so G--E 78 too*., 100' 0001 (9-7< B59 S 11 NON-PHOTOCHEMICALLY REACTIVE The Sherwin-Williams Company Cleveland, Ohio 44101 >1980. The Sherwm-WiHiam* Company SAL 000060942 APPENDIX A-2 Table 4. Estimated consumption of important solvents in paints and coatings.4 Pigments Aliphatic hydrocarbons Methyl ethyl ketone Xylenes Other aromatics Toluene Ethanol Acetone Glycol ethers and ether esters n-Butanol Isopropanol Ethyl acetate Methyl isobutyl ketone Butyl acetates Other ketones and esters Ethylene glycol Propyl acetates Other alcohols Other solvents Propylene glycol Methylene chloride Other glycols Millions of pounds TW'"1974 WT 1976 1977 1603 1375 1280 rrsr-"TT20 380 342 319 345 357 544 435 363 325 300 421 399. 326 305 290 326 250 268 260 255 200 210 200 200 200 200 184 175 190 196 180 194 176 190 195 140 155 135 145 151 121 125 115 120 125 120 103 91 110 no 122 125 103 105 105 93 86 80 84 86 70 75 70 74 75 57 52 48 54 56 60 55 50 53 54 40 42 40 41 41 40 40 36 38 38 30 32 29 33 34 15 15 14 15 15 11111 An Evaluation of Engineering Control Technology for Spray Painting, NIOSH, 1981, p. 12 . SAL 000060943 APPENDIX B METHOTREXATE Tablets end P*r*nwnl* 1 R WARNING METHOTREXATE MUST BE USED ONLY BY PHYSICIANS EXPERIENCED IN ANTIMETABOLITE CHEMOTHER APY. BECAUSE OF THE POSSIBILITY OF FATAL OR SEVERE TOXIC REAC TIONS THE PATIENT SHOULD BE FULLY INFORMED BY THE PHYSI CIAN OF THE RISKS INVOLVED AND SHOULD BE UNDER HIS CONSTANT SUPERVISION. DEATHS HAVE BEEN REPORTED WITH THE USE OF METHOTREXATE IN THE TREATMENT OF PSORIASIS. IN THE TREATMENT OF PSORIASIS METHOTREXATE SHOULD BE RE STRICTED TO SEVERE. RECALCI TRANT, DISABLING, PSORIASIS WHICH IS NOT ADEQUATELY RE SPONSIVE TO OTHER FORMS OF ; THERAPY. BUT ONLY WHEN THE DI AGNOSIS HAS BEEN ESTABLISHED. ' AS BY BIOPSY AND/OR AFTER DER MATOLOGIC CONSULTATION. 1. Methotrexate may produce marked depression of bone marrow, anemia, leukopenia, thrombocytopenia and bleeding. 2. Methotrexate may be hepatotoxic. par ticularly at high dosage or with pro longed therapy. Liver atrophy, necrosis, cirrhosis, fatty changes, and periportal fibrosis have been reported. Since changes may occur without previous Description: Methotrexate Lederle (for merly A-methopteric) is an antirnetabolite used in the treatment of certain neoplastic diseases. Methotrexate Tablets contain 2.5 mg of Metho trexate. Methotrexate Sodium Parenteral is available both in 2.5 mg/ml and 25 mg/ml strengths each available in 2 ml vials. Each 2.5 mg/ml (5.0 mg) rial contains per 2 ml: Methotrexate Sodium equivalent to 5 mg Methotrexate, 0.90% w/v of benryl alcohol as a preservative, and the following Inactive Ingre dients. Sodium Chloride 0.630% w/v and Wa ter for Injection <jb ad 100% V. Sodium Hy droxide to adjust pH to approx. 8.5. Each 25 mg/ml (50 mg) rial contains per 2 ml; Methotrexate Sodium equivalent to 50 mg Methotrexate, 0.90% w/v of benzyl alcohol as a preservative, and the following Inactive Ingre dients: Sodium Chloride 0-260% w/v and Wa ter for Injection qs ad lCO% V. Sodium Hy droxide to adjust pH to approx. 8.5. If desired, the solution may be further diluted with a compatible medium such as Sodium Chloride Injection USP. Storage for 24 hours at a temperature of 21* to 25* C results in a product which is within 90% of label potency, Each 20 mg vial of sterile cryodesiccaied pow der, for single use only, contains: Methotrexate Sodium equivalent to 20 mg Methotrexate. Contains no preservative, with Sodium Hy droxide a# an inactive ingredient. Contains approximately 0.14 milLiequivalenta of sodium per vial. Reconstitute immediately prior to use with 20 ml of an appropriate sterile, preserva tive-free medium eueh as Sodium Chloride In jection, USP. Action: Methotrexate has as its principal mechanism of action Ibe competitive inhibi- Continued on next page SAL 000060944 984 Product Information Always consult Supplement Lederle--Cont. Contraindications: Pregnant psoriatic pa verse reaction. Moet such adverse resetiora^ tients should not receive Methotrexate. Psori reversible if detected early. When such atie patients with severe renal or hepatic disor or reactions do occur, the drug should b* ^ lion of the enzyme folic acid reductase. Folic odd must be reduced to tetrmhydrofolie acid by this enzyme in the process of DNA synthesis end cellular replication. Methotrexate inhibits the reduction of folie acid and interferes with tissue<ell reproduction. Actively proliferating tissues such as malig nant cells, bone morrow, fetal cells, dermal epithelium, buccal and intestinal mucosa and cellsof the urinary bladder are in general more ders should not receive Methotrexate. Psoriatic patients with pre-existing blood dyscrosias, such as bone marrow hypoplasia, leu kopenia, thrombocytopenia or anemia, should not receive Methotrexate. Warnings: See Box Warninfla Precautions: Methotrexate has a high po* tenlial toxicity, usually dove-related. The phy sician should be familiar with the various char acteristics of the drug and its established clini cal usage. Patients undergoing therapy should duced in doeage or discontinued and appL rate corrective measures should be taken, cording to the clinical judgment of the ph*v cian. Reinstitulion of Methotrexate then-, should be carried out with caution, with quale consideration of further need (or tc* drug and alertness as to possible recurrence^ toxicity. Adverse Reactions: The most common id verse reactions include ulcerative stcmatjca, leukopenia, nausea and abdominal disa^. sensitive to this efTeet of Methotrexate. Cellu be subject to appropriate supervision eo that Others reported are malaise, undue fatigva, lar proliferation in malignant tissue is grestar signs or symptoms of possible toxic effects or chills and fever, dizziness and decreased ns than in most normal tissue and thus Metho advene reactions may be detected and evalu tance to infection. In general, the heiderc* trexate may impair malignant growth without ated with minimal delay. Pretreatment and and severity of aide effect* are considered to a* irreversible damage to normal tissues. Orally administered Methotrexate is absorbed rapidly in moat, but not all patients, and re aches peak aenus levels in 1-2 hours. After parenteral injection, peak serum levels are seen in about one-half this period. Approxi mately one-half the absorbed Methotrexate is reversibly bound to serum protein, but ex changee with body fluids easily and diffuses into the body tissue cells Excretion of single daily doses occurs through periodic hematologic studies are essential to the use of Methotrexate in chemotherapy be cause of its common efTeet of hematopoietic suppression. This may occur abruptly and on apparent safe doaage, and any profound drop in blood-cell count indicates immediate stop ping of the drug and appropriate therapy. In patients with malignant disease who have preexising bone marrow aplasia, leukopenia, thrombocytopenia or anemia, the drug should be used with caution, if at all. Methotrexate is excreted principally by the doee-related. Adverse reaction* as reported for the various systemsare as follows: Skin: erythematous rashes, pruritus, orbe*. ria, photosensitivity, depigmentation, tict*. cia, ecchymoeia, telangiectasia, acne, furusc> losia. Lesions of psoriasis may be aggravated by concomitant exposure to ultraviolet radiaom. Blood: bone marrow depression, leuioper.a. thrombocytopenia, anemia, hypogammaglwo. linemia, hemorrhage from various sites, sepocemia. Alimentary System: gingivitis, pharyngitj. the kidneys in amounts from 6594 to B6% or kidneys. Its use in the presence of impaired stomatitis, anorexia, vomiting, diarrhea, beo- higher within 24 hours. Repeated doses daily renal function may result in accumulation of atemeais, rnelena, gastrointestinal uletratio* result in more sustained serum levels and toxic amounts or even additional renal dam and bleeding, enteritis, hepatic toxicity result aome retention of Methotrexate over each 24 age. The patient's renal status should be deter- ing in acute liver atrophy, necrosis, fatty meu- hour period which may result in accumulation mined prior to and during Methotrexate ther morphoeis, periportal fibrosis, or hepatic erof the drug within the tissues. The liver ceils apy and proper caution exercised should signif rhogi* appear to retain certain amounts of the drug icant renal impairment be disclosed. Drug doe-1 Urogenital System!) renal failure, azotemia. for prolonged periods even after a single thera age should be reduced or discontinued until cysutliTKimaron^oerective oogenesis or sper peutic dose. Methotrexate is retained in the renal function is improved or restored. mategenesis, transient oligospermia, mee- presence of impaired renal function and may In general, the following laboratory testa are strual dysfunction; infertility, abortion, fetal increase rapidly in the serum and in the tiseue recommended as part of essential clinical eval defects, severe nephropathy, cells under such conditions. Methotrexate does uation and appropriate monitoring of patients Pulmonary System: Interstitial Pnuaoa> not penetrate the blood cerebrospinal fluid chosen for or receiving Methotrexate therapy: lis. Deaths have been reported and chronic barrier in therapeutic amounts when given complete hemogram; hematocrit; urinalysis; interstitial obstructive pulmonary has orally or parenterally. High concentrations of renal function tests; and liver function tests. A occasionally occurred. the drug when needed may be attained by di chest x-ray is also recommended. The purpose Centra] Nervous System: Headaches, drerw- rect intrathecal administration. is to determine any existing organ dysfunction nesa, blurred vision. Aphasia, hemiporeta. In psoriasis, the rate ofproduction ofepithelial or system impairment. The tests should be per paresis and convulsions have aim occurred cells in the akin is greatly increased over nor- formed prior to therapy, at appropriate periods following administration of Methotrexate. wiyl skin. This differential in reproductive during therapy and alter termination of ther There have been reporta of leucoencephalepa- rijgee is the basis for the use of Methotrexate to apy. It may be useful or important to perform thy following intravenous administration <d c<8)trol the psoriatie process. liver biopsy or bone marrow aspiration studies Methotrexate to patients who have had cranio Indication*: where high dose or long-term therapy is being spinal irradiation. Ariti-neoplsatic Chemotherapy followed. After the intrathecal use of Methotrexate, lie Methotrexate is indicated for the treatment of Methotrexate is bound in part to serum albu central nervous system toxicity which m* gestational choriocarcinoma, and in patients min after absorption and toxicity may be in occur con be classified as follows: (1) ebemxzJ with chorioadenoma destruens and hydatidi- creased because of displacement by certain arachnoiditis manifested by such symptom* ** form mole. drugs such as salicylates, sulfonamides, di- headache, back pain, nuchal rigidity, and fe Methotrexate u indicated for the palliation of phenylhydantOLD. phenylbutazone, and some ver; (2) paresis, usually transient, manifested acute lymphocytic leukemia, it is also indi antibacterials as tetracycline, chlorampheni by paraplegia associated with involvement cated in the treatment and prophylaxis of me col and para-amino-benzoic acid. These drugs, with one or more spinal nerve roots; (3) leoo> ningeal leukemia. Greatest effect has been especially salicylates, phenylbutazone, and encephalopathy manifested by confusion. trr> observed in palliation of acute lymphoblastic sulfonamides, whether antibacterial, hypogly Lability, somnolence, ataxia, dementia, sol (stem-cell) leukemias in children. In combina cemic or diuretic, should not be given concur occasionally major convulsions. tion with other anticancer drugs or suitable rently until the significance of these findings is Other reactions related to or attributed to th* agents Methotrexate may be used for induc established. use of Methotrexate such as metabolic tion of remission, but it is most commonly Vitamin preparations containing folic acid or changes, precipitating diabetes; oeteopcrecc used, as described in the literature, in the its derviatives may alter response* to Methc* cffecLs, abnormal tissue cell change*, and eves maintenance of induced remissions. irexate. sudden death have been reported. Methotrexate may be used alone or in combi Methotrexate should be used with extreme Dosage and Administration: nation with other anticancer agents in the caution in the presence of infection, peptic ul Anti-neoplastic chemotherapy management of breast cancer, epidermoid can cer, ulcerative colitis, debility, and in extreme Oral administration m tablet form is often pre cers of the head and neck, and lung cancer, youth and old age. ferred since absorption is rapid and elTectiv* particularly squamous cell and small cell if profound leukopenia occurs during therapy, serum levels are obtained. Methotrexate types. bacterial infection may occur or become a dium parenteral may be given by intramuaJV- Methotrexate is also effective in the treatment threat. Cessation of the drug and appropriate lar. intravenous, intraarterial or intrstbe=) of the advanced stages (III and IV. Peters Stag ontibiotic therapy is usually indicated. In se route. Initial treatment is usually undertaita ing System) of lymphosarcoma, particularly in vere bone marrow depression, blood or platelet with the patient under hospital core- those case* in children; and in advanced case* transfusions may be necessary. `For conversion of mg/kg b.w. to tng/M3 ** of mycosis fungoidoe. Since it is reported thnl Methotrexate may body surface or the reverae, a ratio of 1-30 l Psoriasis Chtmolherapy (See box wsminp* st have on immunosuppressive action, this factor given ns a guide line. The conversion fz-'tf top of Insert) Because of high risk attending its must be taken into consideration in evaluating varies between 1:20 and l:40dependingon g* use. Methotrexate is only indicated in the the use of the drug where immune responses in and body build. symptomatic control of severe, recalcitrant, a patient may be important or e^aentinl. Choriocnrcinoma and similar trophoblart* disabling psoriasis which is not adequately In alt instances where the use of Methotrexate disenxea: Methotrexate is odministerv-d orally responsive to other forms of therapy, but only is considered for chemotherapy, the physician or intramuscularly in do-e-a of 15 to 30 mg daily tvhrn the diagnosis has been esta bltshciL. as by must evaluate the need and usefulness of the for a 5 day course. Such course* ere usu*bf biopsy and/or after dermatologic consultation. drug against the risks of toxic elfecta or ad repeated for 3 Ui 5 times os required, wiin red SAL 0000609-15 for possible revisions Product Information 985 p.r>y of one or more weeks interposed be* doses of 12 eng persquare meter of body surface 2. Divided oral dose schedule: 2.5 mg at 12 tweefi courses, until any manifesting toxic or in an empirical dose of 15 mg. The solution is hour intervals for three doses or at b hour rymptoma subside. The effectiveness of ther made in a strength of 1 mg per ml as staled apy it ordinarily evaluated by 24 hour quanti above with an appropriate, sterile, preservo- intervals for four doses each week. With this dosage schedule, 30 mg per week tative analysis of urinary chorionic gonadotro pin hormone (CGH), which should return to oflrtnaJ or leaa than SO 111/24 hr. usually after the 3rd or 4th course and usually be followed tya complete resolution of measurable lesions in < to 3 week*. One to two courses of Metho tive-free medium such as Sodium Chloride In jection, USP. For the treatment of meningeal leukemia, Methotrexate is given at interval* of 2 to 5 days. Methotrexate is administered until the cell count of the cerebrospinal fluid returns to should not be exceeded. 3. Daily oral dose schedule: 2.5 mg daily for five days followed by at least a two day rest period. With this dosage schedule, 6.25 mg per day should not be exceeded. SPECIAL NOTE: Available data suggest that trexate after normalization of CGH is usually normal. At this point one additional dose is schedule 3 may carry an increased risk of seri recommended. Before each course of the drug advisable. ous liver pathology. careful clinical assessment is essential. Cyclic For prophylaxia against meningeal leukemia, Dosages in each schedule may be gradually combination therapy of Methotrexate with the dosage is the same as for treatment except adjusted to achieve optimal clinical response, other antitumor drugs has been reported as for the intervals of administration. but not to exceed the maximum slated for each useful. Since hydatidiform mole may On this subject, it is advisable for the physician schedule. precede or be followed by choriocarcinoma, to consult the medical literature. Once optimal clinical response has been prophylactic chemotherapy with Methotrex Large doses may cause convulsions. Untoward achieved, each dosage schedule should be re ate has been recommended. Chorioadenoma side effect* may occur with any given intrathe duced to the lowest possible amount of drug dmtruens is considered to be an invasive form cal injection and are commonly neurological in and to the longest possible rest period. The use of hydatidiform mole. Methotrexate is admin- character. Methotrexate given by intrathecal of Methotrexate may permit the return to con stared in these disease states in doses similar route appears significantly in the systemic ventional topical therapy, which should be to those recommended for choriocarcinoma. circulation and may cause systemic Metho encouraged. Leokemia: acuta lymphatic (lymphoblastic) trexate toxicity. Therefore systemic antileuke Antidote for Overdosage: Leucovorin (cit- in children and young adolescents is mic therapy with the drug should be appropri rovorum factor) is a potent agent for neutraliz the meet responeive to present day chemother ately adjusted, reduced or discontinued. Focal ing the immediate toxic effects of Methotrex* apy. In young adults and older patients, clini luekeroic involvement of the central nervous ate on the hematopoietic system. Where large cal remission is more difficult to obtain end system may not respond to intrathecal chemo dcses or overdoses are given. Calcium Leucovo* early relapse is more common. In chronic lym therapy and is best treated with radiotherapy. rin may be administered by intravenous infu phatic leukemia, the prognosis for adequate Lymphomas: in Burkitt's Tumor, Stages I-II, sion in doses up to 75 mg within 12 hours, fol response is leas encouraging. Methotrexate has produced prolonged remis lowed by 12 mg intramuscularly every 6 hours Methotrexate alone or in combination with sions in some cases. Recommended dosage is 10 for 4 doses. Where average doses of Methotrex smroids was ueed initially for induction of re- to 25 mg per day orally for 4 to 6 days. In stage ate appear to have an adverse effect, 2 to 4 ml misaion of lymphoblastic leukemias. More re III, Methotrexate is commonly given concomi (6 to 12 mg) of Calcium Leucovorin may be cently corticosteroid therapy in combination tantly with other antitumor agents. Treatment given intramuscularly every 6 hours for 4 with etherantileukemic drugs or in cyclic com In all stage* usually consists of several courses doees. In general, where overdosage is sus binations with Methotrexate included appear of the drug interposed with 7 to 10 day rest pe pected, the dose of Leucovorin should be equal to produce rapid and effective remissions. riods. Lymphosarcomas in Stage 111 may re to or higher than the offending dose of Metho When used for induction. Methotrexate in spond to combined drug therapy with Metho trexate and should beet be administered within doses of33 mg/M2 in combination with predni trexate given in doses of 0.625 mg to 2.5 mg/kg the first hour. Use of Calcium Leucovorin after sone 60 mg/M* given daily, produced remis daily, Hodgkin's Disease responds poorly to an hour delay is much less effective. sion in 50% of patienta treated, usually within Methotrexate and to roost types of chemother CAUTION: Pharmacist: Because of its po t period of 4 to 6 week*. Methotrexate alone or apy. tential to cause severe toxicity, Methotrexate ic combination with other agents appears to be Mycosis fungoides: therapy with Methotrex therapy requires close supervision of the pa the drug of choice for securing maintenance of ate appears to produce clinical remissions in tient by the physician. Pharmacists should drug-induced remissions. When remission is one half of the cases treated. Dosage is usually dispense no more than a seven (7) day supply of achieved and supportive care has produced : 2.5 to 10 mg daily by mouth for weeks or the drug at one lime. Refill of such prescrip reaerat clinical Improvement, maintenance months. Dose levels of drug and adjustment of tions should be by direct order (written or oral) therapy is initiated, as follows: Methotrexate is dose regimen by reduction or cessation of drug of the physician only. . jiimlnislered 2 times weekly either by mouth are guided by patient response and hemato-. How Supplied: % intramuscularly in doeesof 30mg/M2. Kh&s logic monitoring. Methotrexate has also been 2.5 mg Tablet*--Bottles of 100. who been given in doses of 2.5 mg/kg intrave given intramuscularly in denes of 50 mg once 2.5 mg per ml--2 ml Vials. nously every 14 days. If and when relapse does . weekly or 25 mg 2 times weekly. 25 mg per ml--2 ml Vials. Incur, reinduction of remission con again usu Psoriasis Chemotherapy 20 mg Vial. ally be obtained by repeating the initial induc TVicpaiienf should be fully informed of the risks Military Depot* tion regimen. Various experts have recently involved and should be under constant supervi 25 mg/ml--2 ml vial introduced a variety of doeage schedules for sion of the physician. NSN 6BO5-01-020-2307 both induction and maintenance of remission Assessment of renal function, liver function, with various combinations of alkylating and and blood elements should be made by history, utifolk agents. Multiple drug therapy with physical examination, and laboratory testa wveral agents, including Methotrexate given (such as CBC, urinalysis, serum creatinine, esaoomitantly is gaining increasing support in liver function studies, and liver biopsy Lf indi both the acute and chronic forms of leukemia. cated) before beginning Methotrexate, periodi The physician should familiarize himself with cally during Methotrexate therapy, and before the new advances in antileukemic therapy. reingtituting Methotrexate therapy after a granulocytic leukemia is rare in chil rest period. A ppropriate steps should be taken dren but common in adults. This form of leuke to avoid conception during and for at least mia responds poorly to chemotherapy and re- eight weeks following Methotrexate therapy. ^`ssiohi are short with relapse* common, and There ere three commonly used general type* t****tsnee to therapy develops rapidly, of doaage schedules: ^uiageal leukemia: Patients with leukemia 1) weekly oral or parenteral intermittent trt subject to leukemic invasion of the central large doses aervotu ryrtem. This may manifest character 2) divided dose intermittent oral schedule ise signs or symptoms or may remain ailent over a 36 hour period ad be diagnosed only by examination of the 3) daily ora! with a rest period ^pirwpinaj fluid which contains leukemic All schedules should bo continually tailored to La such cases. Therefore, the CSF should the individual patient- Dose schedules cited * examined in all leukemic patienta. Since below pertain to an average 70 Kg adult. An f^age of Methotrexate from blood serum to initial lest dose one week prior to initiation of *** wrebrospinal fluid is minimal, for ade- therapy is recommended to detect any idiosyn 4uile tlierapy ihe drug i* administered in- crasy. A sugfjeiried dose range is 5-JO mg parJJ,'^>*caliy. It is now common practice because enteraily. SAL 000060946 Opted increased frequency of meningeol Recommended starling do schedules: uieaiia to administer Methotrexate in- 1. Weekly single oral, JM or IV dcv-e schedule: thetally as prophylaxis in all cases of lym- 10-25 mg per wt^k until adequate response leukemia. is achieved, Wuh this dowige schedule, 50 thecal injection, the sodium salt of mg per week should ordinarily not be ex **'*trat* i* administered in solution in ceeded. CURRENT REPORT EPA CARCINOGEN ASSESSMENT GROUP CARCINOGENS LIST REFERENCED IN CANCER POLICY CANDIDATES NOTICE 305 CHEMICALS HAVING SUBSTANTIAL EVIDENCE OF CARCINOGENICITY* 2-Acetylamino/luorene Acrylonitrile ANatoxins1 Aldrin 4-Aminobiphenyl Amitrole Aramite Arsenic and Arsenic Compounds -f Asbestos -- Auramine and the manufacture of Auramine Azaserine ' Benz(c)acridine - Benz(a)anthracene Benzene Benzidine Benzo(a)pyrene Benzo(b)fluoranthene BenzofjHJuoranthene * Beryllium and Beryllium Compounds N,N*Bis(2-Chloroethyl)*2>NaphthyIamine (Chlor naphazlne) ' Cadmium and Cadmium Compounds Carbon Tetrachloride t Chlorambucil ' Chloroalkyl Ethers Bis(2-chloroethyl) ether (BCEE) Bistchlororr.ethyl) ether (BCME) Chlorometh.W methyl ether (CMME), technical grade Chlordane Chlorinated Ethanes . jL2-Diehloroeihane {Ethylene Chloride; Ethylene Dihloride (EDC)| H Hexachloroethane " 1,1,2.2-Telrachloroethane 1.1.2-Trichloroelhane ` Chlorobenzilale Chloroform Chromium Compounds, Hexavalenl Chrysene ' Citrus Red No. 2 Cool Tar and Soot Coke Oven Emissions (PolycyclicOrganic Matter (POM)J Creosote Cycnsin Cyclophosphamide * Dounomydn ' .. DDT (DichlorodiphenyUrichloroethane) Rinllale ' Dibenzfa.hiacridine Dibenzfn.j L-uTidine , Dibcn7.fa.h)onlhracene ` 7M-Dibcnzoi'c,R)corbazo)e Dibenzofa.eipyrcne Di benzol a.bipyrene Dibcnznf a.i jpyrene 1.2-Dibromo-3-chloropropnne (DBCP) 1.2-Dibromnethane JElhylene Bromide, Ethylene Dibrornidc (EUB)| 3.3' Dichlorobenzidine (DCB) Dicldrin Dicpoxybutane 1.2-Diethylhydrazlne Diethylstilbcstrol (DES) Dihydrosafrole 3.3'-Dimethoxybenzidine (o-Dianisidine) p-Dimelhylaminoazobenzene 7.12-L)imclhylben7.(a tanlhraccne 3.3'-Dinie thy! benzidine (n-Tolidino) Dimelhylcarbamoyl Chloride 1.1- Dimelhylhydrazine 1.2- Dimelhylhydrazine Dimethyl Sulfate ' ' Z/4-Drnilrololuene 1,4-Dinxane 1.2- Diphenylhydrazine Epichlorohydrin Ethylcnehisdithiocarbamate (EBDC) Elhyleneimine (Aziridine) * Ethylene Oxide Elhylenelhiourea Ethyl MethanesuMonale Formaldehyde Clycidaldehyde Heplacldor Hexachlorobenzene Hcxachlornbuladiene Hcx^cldorocyclohexane (HCH) HvdrvUinc j- IndenoU.2,3-cd)pyrcn^`| Iron Dcxlran Isosafrolc Kepone (Chlordecone) Lasiocarpine Melphalan J. Mcthapyrllene 1 3- Methylcholanl hrene 4,4'-Melhylenebis(2-Cliloroaniline) (MOCA) Methyl Iodide Methyl Melhanesulfonate N-Mclhyl-N'-mtro-N-nitrosoguanidine Mclhyllhiour'acil * Mitomycin C 1 Mustard Gas 1- Naphthylamine. technical grade 2- Naphlhy!amine Nickel and Nickel Compounds Nitrogen Mustard and its hydrochloride Nitrogen Mustard N-oxide and its hydrochloride 5-Nitro-o-loluidine 4- Nilroquinoline-l -oxide Nitrosaminrs N-NilrnsodieHinnolamlne N-NilrnsndicthyInn tine (DKNA) N-Nitrosodimeihylamine (DMNA) N-Nitrosodi-n-bulylamine N-Nilrosodi-n-propylamine SA!- 000060947 N-Nilrosomclhylelhyjamine N-Nilrosomelhvlvinylnmine N-Ni troso-N Ethy 1 urea (NED) N-Nilroso-N-Molhylnrea (NMU) N-Nilroso-N-inet hylurelhano N-Nilrosomnrph'!ine N-Ni trosonor nicotine b 14-nn 0(P........ liv tKf OUBEAU fJAIlOMAl A f T A O C. INC C,a$m IN 1 QN DC ?00I)7 306 Nilrosanines (continued) N-Nttrosopipendine N-Nitrosopyrrolidine N-Nitrososarcosine Pcnlachloronitrobenzene Phcnncetin ** Polychlorinated Biphenyls (PCBs) Pronomide 1,3-Propane Sultone B-Propiolaclone Propylthiouracil' Reserpine * * This is not a comprehensive list of all chemicals having substan tial evidence of carcinogenicity. Other chemicals will be added. No attempt has been made to select chemicals based upon ap propriateness for regulation by EPA, The list is intended to be a oasis for selection by the various program offices according to their specific needs. * Fungal toxin, not an industrially manufactured products * Used as a drug. Evaluated by lARC. as not having sufficient evidence of car cinogenicity. 1 Used as a food. * OCCUPATIONAL SAFETY & HEALTH REPORTER Saccharin * Safrole ' Selenium Sulfide Streplozolocin ' 2.3.7.8-Telmchlorodibenzo-p-dioxui (TCDD) Tetrachloroethvlene (Pcrchloroclnylene) Thioacelamide Thiourea o-Toluidine Hydrochloride Toxaphene Trichloroethylene 2,4,6-Trichlorophcnol . Tris (I-?i7iridinyl)phosphine sulfide (Thio-TEPA)' Tris(2,3-dibrom'.propyl)phoFphate Tris(2,3-dibromopropyl)phosjjtoate Trypan Blue, commercial grade Uracil Mustard * ' Urethane (Ethyl caihamate: ethyl ester of carbamic acid) Vinyl Chloride Vinylidene Chloride' nfc |f ^ 000060948 |i! t.i Li ^ _ n r\nr~:\l--N.n/7":--\rz J j- K O- ' \! ( L! 3 \ ' /{ ij t\ \ ' -3i - 'V"> L--^UCL.ViJ V ..SC' ~f: j--? i / V.J V. ^ i.j xALJ A NEWS AFRICAN SPECIAL REPORT . Why was an unskilled drifter hired to clean deadly chemicals that trained employees wouldn't touch? Why wasn't his family told of his death? f XfCl- I ,Vi'^j n , li CcnrxG <T.:*?caJ Plant W0, i-h wm c&v!^ lilt -v ;V-" !ii; ,,f,li' t: r< *-* : ` , ' ---f* -p,-iVv-yX--'W.*<.!*.( f ( . t I. M. I i l. , l -: s: ka. %iLAjfra|V ;' y i ? ^ il 1 i j\v C\ \l\ I <! (0g$f \ >v--;> / .., -v^ .r_-- - pX Xv-- 7Tv* Xirv+rl-cjfi -- THE SCENE: Sketch shows how Linwood Bryant died at Ccnocc's Fairfield plan*. Bryant is profiled on 1QA. >rj/_ Q0o 609 49 I The hospital's diagnosis City Ambulance No. fi took Bryant's three fellow workers to South Baltimore General Hospital. Doctors at the emergency room examined them and determined that they had been ex posed to noxious fumes. The official diagno sis: "acute hydrocarbon exposure." Another .ambulance carried Bryant to the hospital. He was pronounced dead there at 2:45 p.m. His body was sent to the state Medical Examiner's Office for an autopsy, where it was determined that he died from acute benzene poisoning. '. No blood or urine tests were conducted on any of the three workers -- an omission that later led MOSH consultant Dr. Ziem to send a` letter criticizing South Baltimore General's handling of the case. According to Dr. Ziem. without blood and urine samples doctors could not have deter mined whether the laborers had sustained damage to their bone marrow. And because1 benzene is a known cause of leukemia, a can cer that attracks bone marrow, those tests should have been performed. Dr. Ziem says. ' "It's gcod medical practice to document it; to see whether there was any effect on the bone marrow," says Dr. Ziem. who is a rec-. ognized expert on occupational disease. "And if there was, then one would want to watch them (those exposed) more closely," But the chief of emergency services at South Baltimore General, Dr, Jean Thorne, says blood and urine tests were not per formed on the three workers because doctors were not aware at that time that they had been exposed to benzene. "These men came in and said they had been exposed to gas. But they had no idea what type of gas. They had no severe symp toms," Dr. Thome says. "From a practical standpoint, we can't run all kinds of tests on everyone who comes in saying they were ex posed to gases. We get those cases all the time. Sometimes companies will send us a roomful of workers who might have been ex posed. In 9S percent of the cases, there's noth ing wrong. "We observed them (Reeves, Washington and Grant) for several hours to see if they had any latent symptoms betore letting them go." In the meantime, Joseph, Pilkerton, man ager of the Baltimore PeaWoad office and the man who hired Bryant and the other three workers, had notified MOSH of the accident. When MOSH industrial hygienists LeClair and Jay Rupp checked Tank 152 a few hours after their 5:30 p.m. arrival at Conoco, the air blower on the tank's top hatch was not work- mg. But Conoco company officials have told MOSH that it was on while the workers were inside. Air samples taken by LeClair and Rupp inside the tank showed concentrations of ben zene from 500 to 1,000 parts per million. The allowed level is 50 parts per million. Safety officials say that with the level of benzene in the tank, the Norton 7500-30 respi rators the workers were issued -- which only filter air in the tank before it is inhaled -- were virtually useless in the tank. More ex pensive respirators connected to an oxygen source outside the tank would have proably prevented Bryant's death, MOSH officers say. Even when Rupp and LeClair took air samples with the fan working, tests indicated the benzene inside the tank atmosphere was at least double the level that the respirators could have safely handled. And, say state safely investigators, nei- thcr Chesapeake nor Pcakload officials suffi ciently trained the four laborers in how to use the respirators. If the workers had received proper instructions, safety officials say, thev would have known that smelling fumes while wear ing the masks was an indication that they were being poisoned. WViethi'f tl-fl ;>ir licr that day by Conoco was legally sufficient is a matter of de-lute. According to LrClam, current state stan dards require (hat a company take an air sample from, invade a tank D.-mrc workers en ter. Bui ili*- s! .lie I.t: d i do iva * p--r :fic.iIv stale that au u.roognoiu the tank be tesd, LeClair says, t U tt i O.r rj.'*$ Op*. .'1 c--zap r-" U'<^ fl >1 v i -; Li ks-i v^j \* iJ P^lbnmir U '^*1 Ncrs^ J ^'ti e Copyright 1831 The Newt Afrwrican By Lorry Lewis and Joe Ca!derone News American Staff On the morning of Aug. 6, 19S0, Linwood Bry ant, 40, was hired by a temporary labor agency to - dean a south Baltimore chemical tank that coni tained benzene residue, a deadly organic chemi: chi distilled from petroleum. That afternoon, he was pronounced dead of chemical poisoning at South Baltimore General Hospital. Bryant was an unemployed drifter -- a tem porary laborer who was staying at a city mission for the homeless. He had received virtually no . training, enjoyed no union protection, was entitled to no benefits from his employer. Until last week, his family didn't even know he was dead. He had been hired by a labor subcontractor -- . the kind of company Baltimore industrial and manufacturing concerns are increasingly turning to for help in performing hazardous tasks that full-time employees cannot or will not perform. The practice, say safety officials, exposes un trained, temporary workers to dangerous situa tions and has resulted in at least two deaths in re- \ * v "i ,/ < _ /' , e '*** '* ^ ; -v- LINWOOD BRYANT: Shown in old photo. cent months. It also permits manufacturing and industrial concerns to sidestep legal responsibility for accidents and injuries. A A'etrs American inquiry uncovered these facts about Linwood Bryant's employment, the 'accident that led to his death, and the owing practice of hiring labor subcontractors for hazard ous tasks: Bryant and his three co-workers were sent into the chemical tank despite the fact that em ployees of Conoco Inc., the owner of the tank, re fused to do the work because they feared it was too dangerous. See WORKERS, 10A, % yi- WORKERS from 1A* 1 * * * V Bryant, according to safety officials, Nvas given inadequate equipment and training for the task, 1 In violation of state and federal work jaws, a 14-year-old youth was permitted to work beside Bryant in the chemical tank. ` Six months after he died, Bryant's rela- lives in New York still had not been notifed of his death either by the police or by the thre^ companies that directly or indirectly employed him, even though News American reporters Were able to locate the family after trying for only several hours. The three workers who survived the ac cident were not tested to determine the ef fects of the chemical exposure on their health, and did not receive medical examina tions until more than a day after the accident. 0Maryland law permits companies that subcontract work to escape liability for acci dents and deaths that occur on their'properties, a major factor in the increasing use of subcon tractors and temporary employees to do spe cialized and hazardous work. - As a temporary employee, Bryant received the minimum wage. Sh.10 an hour. Like many day laborers, his working conditions are loosely regulated by state and federal agencies. No gov- emment agency keeps statistics on how many temporary laborers are injured or killed in Bal timore or in Maryland, or even on how many there are. .. Despite increasing government regulation of safety and the workplace, there isn't even a pre cise definition of what a day laborer is. Anyone who calls himself a day laborer is one -- like linwrxxj Bryant. .The practice of hiring subcontractors for sTv>riaii7w1 and dangerous work is increasing fur many reason';, sav occupational sifety exports such as Dr. Gi.ice'Ziem. a physi cian and a consult.tut :o the Maryland Occupa tional Safety and Health aivncy; Harvey Up- Mt-in, commissioner of MaiTland'-' Division of I-d..r and hnlu.'ty ard pr.-'i.!. nt <4 a naii.nn! f; - of -a.m- (<eoi|- :'in;:.i| s.-.iriy a.-'Ticies; and p.\p wpi.on. prt-.e' L:--d .v*`lwuikers (if [>.,! a I -..;! V \ : : di.in f-ty r -e-. leader ; - Because unionized workers are increasingly reluctant to perform potentially hazardous jobs without special training and equipment, the ex perts say, some companies hire non-union work ers for temporary work in an effort to save money. -. Another reason companies sometimes hire labor subcontractors for hazardous work is that state law places responsibility for the health and safety of the workers on the firm that pays their salary -- regardless of for whom the work actually is being done. Wn 'fact, Maryland law does not require a company that hires a subcontractor to tell the subcontractor that a job might be dangerous or involve hazardous materials. . ; Although subcontractors sometimes bring expertise to the handling of such jobs, more fre quently they do hazardous tasks as inexpensive ly and quickly as possible, often endangering workers, say Dr. Ziem and Wilson. In another Industrial death last July 24 in volving a subcontractor, 20-year-oId Mark Jones suffocated when he was lowered into a gratn storage bin at Locust Point. The bin, owned by Indiana Grain Co., had not been tested for oxy gen content before Jones entered, MOSH inspectore charge. .Jones worked for the Davco Corp., a Ten nessee-based subcontractor hired by Indiana Grain to renovate its Baltimore grain storage facilities,. When he was killed, Jones was doing a job normally performed by Indiana Grain Co, em ployees, who were on strike at the lime. MOSH officials have recommended that the Davco Corp, be fined 15,500. Under Maryland law. Indiana Gram is not responsible for the death because the company, like Conoco, find hired a subcontractor. Dr. Ziem says more find more companies are using temporary laborers as "disposable people" to fvrimm hazardous tasks, "WTu-n a comjvuiy warns dmy work done, they cn!( us,'* says Frank ly-uunnn, a member Of the ofiH'C St.iff ;U Jnc., ihc C'Mipmy that lun-d Bryujii. gt-i (he worst 0000609S1 Hs' r` a Tj v 1 C* *"'./ v fVSr.V 1 i- Lu hi ;y> \ -**- < vj J.', P\ ^ /**, r* /^s, r.s.-fH ^eJ` ii V' isj-7jy2 ^ ~ /rrs r kiI;i iU\jis;JMm(i np nr rs^i^ry 10.ra ^'T'vfFfCi u!;W'fctf>'W W Vsii U N?U .v3 pH 5 n / v j r -3 >>-^v ': :\)\?Ui 8 l iGlIrw `The law encourages subcontracting out of hazardous work," Dr. Ziem says, "If you're a large company and you subcontract a job out, first of all it's a way to get cheap labor, and if someone gets hurt, they can't file for work man's compensation against you. Unless the primary employer can be held responsible, we're going to see mere of this." ; According to Frank Morgan,'chief of MOSH: "Temporary laborers are usually not Uic type of people who can demand safety and\ health conditions be met. "Economically, most of the temporary peo*. pie desperately nc-cd the money to live on a day. to-day basis, so they're not about to refuse a job, even if it mi^ht be hazardous. And they're not organized so they have no union speaking in their behalf. Most of the time, they don't have the knowledge or education to be aware of hazards. "They're not the type of workers who are about to demand changes. It's a situation that's ripe for ex-ploitation of the workers." ' The Rev. Wade Dryden, director of the Helping Up Mission where Bryant spent his last night, says that the day laborers "are used and used and'used. There's always somebody else to take their place. : "They get the dirty jobs union men won't do. Union men get $10 an hour, These men get the minimum wage." Why Bryant riic-d The story of Linwood Bryant and Tank 152 boils down to this: '""Conoco used the tank to store chemicals. When the company's own employees refused to clean the tank -- fearing the homes that had pccumulatcd inside -- Conoco turned to a subcontractor, Chesapeake Environmental Inc., which went to Pcakload Labor for the workers to do the job. V__ /'Pcakload hired Linwood Bryant, two oth er men and a 14-year-old to go into the tank with respirator gas masks. Two of the work ers were wearing shorts. Within two hours, Linwood Bryant was dead, according to an autopsy, of acute ben zene chemical poisoning. What follows are the events that led to Linwood Bryant's death and the aftermath, reconstructed from interviews with his co workers, workers at the Conoco chemical plant, safety ar.d MOSH officials, his employ ers, police and family members: Deadly benzene " \ According tn 6', ark Edm^Ads, a Conoco ---e--m--p--l-oy1_e_e_f_o_r _se_v_e_h'years an/d.a union official, Tank 152 had !/>?n used to store Nalkvlene, a form of the chemical benzene that is the ac tive ingredient in soap detergents. It :s also very dangerous and is known to cause cancer and damage the body's central neivous system. The tank, which sits amid a 73-acre field of tanks and auaxcring p:p"s. is ntviui .V) fivt high and 2h fix ( in diameter and is painted yc.. w. Hcwnr-c the f .I'm nf Nalkylene stored in Tank 1.-2 would is.: (Jix'oiv.jvim? naiurnlly. the comp.ti-y st'j'j-'i 'ihm; u ;.yw.Tal years ape. Sir,, r th' u, IV. a ,-ays, the part of the plan: w lOTt lai.V; la.' has team shut d ;i .. ' :.`l . fl "lu i henucjl .ti`. ,-..j 11f.avc; tv.;i, s'oriij in j.mk 152. OV k iV k 1 * iC HA ( r W .*/, \ *.,1 v .o clean Tank 152. Although the company will not discuss the tank or the accident that oc curred there, Edmunds says he and two sum mer workers refusvd to clean it because he believed the fumes inside were too dangerous. "My supervisor told me there was three or four inches left in the bottom of the tank," Edmunds says. "But it was still knee-deep in there. And you could smell the fumes as soon as you get near the tank." Edmunds say he reported to his superiors that the job was too dangerous, and he was given another assignment for the day. Then, about a month before the accident, Conoco made an attempt to clear the tank of gas. The tank was flooding with hot water and steam, drained and again filled with steam -- a procedure that continued for the next 18 days. And about 12 days before the accident, Conoco installed a fan-like "air mover" to the top hatch of the tank in an attempt to draw fresh air into it before workers went inside. Conoco had gotten Chesapeake Environ mental, a firm with an office at 8123 Pulaski Highway that specializes in environmental cleanup, to undertake the cleanup. On Aiig. 5, four workers from Anybody Anytime Inc., an other temporary labor agency, worked clean ing the tank. According to MOSH officials, three of the same workers and another temporary em ployee returned the next morning but were dismissed shortly after they began work be cause George Crowley of Chesapeake says they appeared drunk -- symptoms identical to those of benzene poisoning. Crowley then called Peakload to get an other cleanup crew. On both mornings, Conoco had tested the air inside Tank 152 and determined that there were no toxic fumes present and that the oxy gen was sufficient. But, safety inspectors say, the tests were inadequate because the air sampled was within the area where the fan had created only a narrow column of air flowing from the bottom hatch to the top manhole -- without I circulating air to any other areas. r Most of the atmosphere inside the tank away from the entrance holes remained stag nant and heavily laced with benzene, state safety officials say. A thorough test of the air inside the tank would likely have revealed that it could kill workers wearing the kind of respirators is-^ sued to the four workers, says Ron LeClair, ir state industrial hygienist with MOSH. And, according to LeClair, no further tests, of the air were done while the men were working in the sludge -- an activity LeClair says would have increased the level of ben zene in the tank's atmosphere. Inside the tank, Bryant and the three oth er workers -- Milton Gram, 21, Bernard Washington, 20, Raymond Reeves, 14 -- pushed the sludge with shovels and sponge mops, attempting to get it to a pump that would push it through a hose to a truck outside. While in the tank, two or three of the day laborers reported that they complained of headaches and dizziness,. MOSH investigators say. Crowley told MOSH investigators that the workers did not tell him of such problems. After taking a break, the men re-entered the tank, but again complained of fumes and were attempting to get out when Bryant slipped and fell into the sludge, Reeves and Grant say. They and Crowley began pulling Bryant's unconscious body from the lank porthole. Two Conoco workers ran toward the tank and Edmunds followed them. "He was covered with that sludge." Ed munds says. "V.'e had to wipe it away from his eyes, nose, mouth and cal's. His eyes were open', but he was completely limp." * SAL 000060952 ?