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Recognition of Hazards

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A workplace hazard can be defined as any condition that may adversely affect the well-being or health of exposed persons. Recognition of hazards in any occupational activity involves characterization of the workplace by identifying hazardous agents and groups of workers potentially exposed to these hazards. The hazards might be of chemical, biological or physical origin (see table 1). Some hazards in the work environment are easy to recognize—for example, irritants, which have an immediate irritating effect after skin exposure or inhalation. Others are not so easy to recognize—for example, chemicals which are accidentally formed and have no warning properties. Some agents like metals (e.g., lead, mercury, cadmium, manganese), which may cause injury after several years of exposure, might be easy to identify if you are aware of the risk. A toxic agent may not constitute a hazard at low concentrations or if no one is exposed. Basic to the recognition of hazards are identification of possible agents at the workplace, knowledge about health risks of these agents and awareness of possible exposure situations.

Table 1.  Hazards of chemical, biological and physical agents.

Type of hazard

Description

Examples

CHEMICAL

HAZARDS

 

Chemicals enter the body principally through inhalation, skin absorption or ingestion. The toxic effect might be acute, chronic or both.,

 

Corrosion

Corrosive chemicals actually cause tissue destruction at the site of contact. Skin, eyes and digestive system are the most commonly affected parts of the body.

Concentrated acids and alkalis, phosphorus

Irritation

Irritants cause inflammation of tissues where they are deposited. Skin irritants may cause reactions like eczema or dermatitis. Severe respiratory irritants might cause shortness of breath, inflammatory responses and oedema.

Skin: acids, alkalis, solvents, oils Respiratory: aldehydes, alkaline dusts, ammonia, nitrogendioxide, phosgene, chlorine, bromine, ozone

Allergic reactions

Chemical allergens or sensitizers can cause skin or respiratory allergic reactions.

Skin: colophony (rosin), formaldehyde, metals like chromium or nickel, some organic dyes, epoxy hardeners, turpentine

Respiratory: isocyanates, fibre-reactive dyes, formaldehyde, many tropical wood dusts, nickel

 

Asphyxiation

Asphyxiants exert their effects by interfering with the oxygenation of the tissues. Simple asphyxiants are inert gases that dilute the available atmospheric oxygen below the level required to support life. Oxygen-deficient atmospheres may occur in tanks, holds of ships, silos or mines. Oxygen concentration in air should never be below 19.5% by volume. Chemical asphyxiants prevent oxygen transport and the normal oxygenation of blood or prevent normal oxygenation of tissues.

Simple asphyxiants: methane, ethane, hydrogen, helium

Chemical asphyxiants: carbon monoxide, nitrobenzene, hydrogencyanide, hydrogen sulphide

 

Cancer

Known human carcinogens are chemicals that have been clearly demonstrated to cause cancer in humans. Probable human carcinogens are chemicals that have been clearly demonstrated to cause cancer in animals or the evidence is not definite in humans. Soot and coal tars were the first chemicals suspected to cause cancer.

Known: benzene (leukaemia); vinyl chloride (liver angio-sarcoma); 2-naphthylamine, benzidine (bladder cancer); asbestos (lung cancer, mesothelioma); hardwood dust (nasalor nasal sinus adenocarcinoma) Probable: formaldehyde, carbon tetrachloride, dichromates, beryllium

Reproductive

effects

 

Reproductive toxicants interfere with reproductive or sexual functioning of an individual.

Manganese, carbon disulphide, monomethyl and ethyl ethers of ethylene glycol, mercury

 

Developmental toxicants are agents that may cause an adverse effect in offspring of exposed persons; for example, birth defects. Embryotoxic or foetotoxic chemicals can cause spontaneous abortions or miscarriages.

Organic mercury compounds, carbon monoxide, lead, thalidomide, solvents

Systemic

poisons

 

Systemic poisons are agents that cause injury to particular organs or body systems.

Brain: solvents, lead, mercury, manganese

Peripheral nervous system: n-hexane, lead, arsenic, carbon disulphide

Blood-forming system: benzene, ethylene glycol ethers

Kidneys: cadmium, lead, mercury, chlorinated hydrocarbons

Lungs: silica, asbestos, coal dust (pneumoconiosis)

 

 

 

 

BIOLOGICAL

HAZARDS

 

Biological hazards can be defined as organic dusts originating from different sources of biological origin such as virus, bacteria, fungi, proteins from animals or substances from plants such as degradation products of natural fibres. The aetiological agent might be derived from a viable organism or from contaminants or constitute a specific component in the dust. Biological hazards are grouped into infectious and non-infectious agents. Non-infectious hazards can be further divided into viable organisms, biogenic toxins and biogenic allergens.

 

Infectious hazards

Occupational diseases from infectious agents are relatively uncommon. Workers at risk include employees at hospitals, laboratory workers, farmers, slaughterhouse workers, veterinarians, zoo keepers and cooks. Susceptibility is very variable (e.g., persons treated with immunodepressing drugs will have a high sensitivity).

Hepatitis B, tuberculosis, anthrax, brucella, tetanus, chlamydia psittaci, salmonella

Viable organisms and biogenic toxins

Viable organisms include fungi, spores and mycotoxins; biogenic toxins include endotoxins, aflatoxin and bacteria. The products of bacterial and fungal metabolism are complex and numerous and affected by temperature, humidity and kind of substrate on which they grow. Chemically they might consist of proteins, lipoproteins or mucopolysaccharides. Examples are Gram positive and Gram negative bacteria and moulds. Workers at risk include cotton mill workers, hemp and flax workers, sewage and sludge treatment workers, grain silo workers.

Byssinosis, “grain fever”, Legionnaire’s disease

Biogenic allergens

Biogenic allergens include fungi, animal-derived proteins, terpenes, storage mites and enzymes. A considerable part of the biogenic allergens in agriculture comes from proteins from animal skin, hair from furs and protein from the faecal material and urine. Allergens might be found in many industrial environments, such as fermentation processes, drug production, bakeries, paper production, wood processing (saw mills, production, manufacturing) as well as in bio-technology (enzyme and vaccine production, tissue culture) and spice production. In sensitized persons, exposure to the allergic agents may induce allergic symptoms such as allergic rhinitis, conjunctivitis or asthma. Allergic alveolitis is characterized by acute respiratory symptoms like cough, chills, fever, headache and pain in the muscles, which might lead to chronic lung fibrosis.

Occupational asthma: wool, furs, wheat grain, flour, red cedar, garlic powder

Allergic alveolitis: farmer’s disease, bagassosis, “bird fancier’s disease”, humidifier fever, sequoiosis

 

PHYSICAL HAZARDS

 

 

Noise

Noise is considered as any unwanted sound that may adversely affect the health and well-being of individuals or populations. Aspects of noise hazards include total energy of the sound, frequency distribution, duration of exposure and impulsive noise. Hearing acuity is generally affected first with a loss or dip at 4000 Hz followed by losses in the frequency range from 2000 to 6000 Hz. Noise might result in acute effects like communication problems, decreased concentration, sleepiness and as a consequence interference with job performance. Exposure to high levels of noise (usually above 85 dBA) or impulsive noise (about 140 dBC) over a significant period of time may cause both temporary and chronic hearing loss. Permanent hearing loss is the most common occupational disease in compensation claims.

Foundries, woodworking, textile mills, metalworking

Vibration

Vibration has several parameters in common with noise-frequency, amplitude, duration of exposure and whether it is continuous or intermittent. Method of operation and skilfulness of the operator seem to play an important role in the development of harmful effects of vibration. Manual work using powered tools is associated with symptoms of peripheral circulatory disturbance known as “Raynaud’s phenomenon” or “vibration-induced white fingers” (VWF). Vibrating tools may also affect the peripheral nervous system and the musculo-skeletal system with reduced grip strength, low back pain and degenerative back disorders.

Contract machines, mining loaders, fork-lift trucks, pneumatic tools, chain saws

Ionizing

radiation

 

The most important chronic effect of ionizing radiation is cancer, including leukaemia. Overexposure from comparatively low levels of radiation have been associated with dermatitis of the hand and effects on the haematological system. Processes or activities which might give excessive exposure to ionizing radiation are very restricted and regulated.

Nuclear reactors, medical and dental x-ray tubes, particle accelerators, radioisotopes

Non-ionizing

radiation

 

Non-ionizing radiation consists of ultraviolet radiation, visible radiation, infrared, lasers, electromagnetic fields (microwaves and radio frequency) and extreme low frequency radiation. IR radiation might cause cataracts. High-powered lasers may cause eye and skin damage. There is an increasing concern about exposure to low levels of electromagnetic fields as a cause of cancer and as a potential cause of adverse reproductive outcomes among women, especially from exposure to video display units. The question about a causal link to cancer is not yet answered. Recent reviews of available scientific knowledge generally conclude that there is no association between use of VDUs and adverse reproductive outcome.

Ultraviolet radiation: arc welding and cutting; UV curing of inks, glues, paints, etc.; disinfection; product control

Infrared radiation: furnaces, glassblowing

Lasers: communications, surgery, construction

 

 

 

Identification and Classification of Hazards

Before any occupational hygiene investigation is performed the purpose must be clearly defined. The purpose of an occupational hygiene investigation might be to identify possible hazards, to evaluate existing risks at the workplace, to prove compliance with regulatory requirements, to evaluate control measures or to assess exposure with regard to an epidemiological survey. This article is restricted to programmes aimed at identification and classification of hazards at the workplace. Many models or techniques have been developed to identify and evaluate hazards in the working environment. They differ in complexity, from simple checklists, preliminary industrial hygiene surveys, job-exposure matrices and hazard and operability studies to job exposure profiles and work surveillance programmes (Renes 1978; Gressel and Gideon 1991; Holzner, Hirsh and Perper 1993; Goldberg et al. 1993; Bouyer and Hémon 1993; Panett, Coggon and Acheson 1985; Tait 1992). No single technique is a clear choice for everyone, but all techniques have parts which are useful in any investigation. The usefulness of the models also depends on the purpose of the investigation, size of workplace, type of production and activity as well as complexity of operations.

Identification and classification of hazards can be divided into three basic elements: workplace characterization, exposure pattern and hazard evaluation.

Workplace characterization

A workplace might have from a few employees up to several thousands and have different activities (e.g., production plants, construction sites, office buildings, hospitals or farms). At a workplace different activities can be localized to special areas such as departments or sections. In an industrial process, different stages and operations can be identified as production is followed from raw materials to finished products.

Detailed information should be obtained about processes, operations or other activities of interest, to identify agents utilized, including raw materials, materials handled or added in the process, primary products, intermediates, final products, reaction products and by-products. Additives and catalysts in a process might also be of interest to identify. Raw material or added material which has been identified only by trade name must be evaluated by chemical composition. Information or safety data sheets should be available from manufacturer or supplier.

Some stages in a process might take place in a closed system without anyone exposed, except during maintenance work or process failure. These events should be recognized and precautions taken to prevent exposure to hazardous agents. Other processes take place in open systems, which are provided with or without local exhaust ventilation. A general description of the ventilation system should be provided, including local exhaust system.

When possible, hazards should be identified in the planning or design of new plants or processes, when changes can be made at an early stage and hazards might be anticipated and avoided. Conditions and procedures that may deviate from the intended design must be identified and evaluated in the process state. Recognition of hazards should also include emissions to the external environment and waste materials. Facility locations, operations, emission sources and agents should be grouped together in a systematic way to form recognizable units in the further analysis of potential exposure. In each unit, operations and agents should be grouped according to health effects of the agents and estimation of emitted amounts to the work environment.

Exposure patterns

The main exposure routes for chemical and biological agents are inhalation and dermal uptake or incidentally by ingestion. The exposure pattern depends on frequency of contact with the hazards, intensity of exposure and time of exposure. Working tasks have to be systematically examined. It is important not only to study work manuals but to look at what actually happens at the workplace. Workers might be directly exposed as a result of actually performing tasks, or be indirectly exposed because they are located in the same general area or location as the source of exposure. It might be necessary to start by focusing on working tasks with high potential to cause harm even if the exposure is of short duration. Non-routine and intermittent operations (e.g., maintenance, cleaning and changes in production cycles) have to be considered. Working tasks and situations might also vary throughout the year.

Within the same job title exposure or uptake might differ because some workers wear protective equipment and others do not. In large plants, recognition of hazards or a qualitative hazard evaluation very seldom can be performed for every single worker. Therefore workers with similar working tasks have to be classified in the same exposure group. Differences in working tasks, work techniques and work time will result in considerably different exposure and have to be considered. Persons working outdoors and those working without local exhaust ventilation have been shown to have a larger day-to-day variability than groups working indoors with local exhaust ventilation (Kromhout, Symanski and Rappaport 1993). Work processes, agents applied for that process/job or different tasks within a job title might be used, instead of the job title, to characterize groups with similar exposure. Within the groups, workers potentially exposed must be identified and classified according to hazardous agents, routes of exposure, health effects of the agents, frequency of contact with the hazards, intensity and time of exposure. Different exposure groups should be ranked according to hazardous agents and estimated exposure in order to determine workers at greatest risk.

Qualitative hazard evaluation

Possible health effects of chemical, biological and physical agents present at the workplace should be based on an evaluation of available epidemiological, toxicological, clinical and environmental research. Up-to-date information about health hazards for products or agents used at the workplace should be obtained from health and safety journals, databases on toxicity and health effects, and relevant scientific and technical literature.

Material Safety Data Sheets (MSDSs) should if necessary be updated. Data Sheets document percentages of hazardous ingredients together with the Chemical Abstracts Service chemical identifier, the CAS-number, and threshold limit value (TLV), if any. They also contain information about health hazards, protective equipment, preventive actions, manufacturer or supplier, and so on. Sometimes the ingredients reported are rather rudimentary and have to be supplemented with more detailed information.

Monitored data and records of measurements should be studied. Agents with TLVs provide general guidance in deciding whether the situation is acceptable or not, although there must be allowance for possible interactions when workers are exposed to several chemicals. Within and between different exposure groups, workers should be ranked according to health effects of agents present and estimated exposure (e.g., from slight health effects and low exposure to severe health effects and estimated high exposure). Those with the highest ranks deserve highest priority. Before any prevention activities start it might be necessary to perform an exposure monitoring programme. All results should be documented and easily attainable. A working scheme is illustrated in figure 1.

Figure 1. Elements of risk assessment

IHY010F3

In occupational hygiene investigations the hazards to the outdoor environment (e.g., pollution and greenhouse effects as well as effects on the ozone layer) might also be considered.

Chemical, Biological and Physical Agents

Hazards might be of chemical, biological or physical origin. In this section and in table 1 a brief description of the various hazards will be given together with examples of environments or activities where they will be found (Casarett 1980; International Congress on Occupational Health 1985; Jacobs 1992; Leidel, Busch and Lynch 1977; Olishifski 1988; Rylander 1994). More detailed information will be found elsewhere in this Encyclopaedia.

Chemical agents

Chemicals can be grouped into gases, vapours, liquids and aerosols (dusts, fumes, mists).

Gases

Gases are substances that can be changed to liquid or solid state only by the combined effects of increased pressure and decreased temperature. Handling gases always implies risk of exposure unless they are processed in closed systems. Gases in containers or distribution pipes might accidentally leak. In processes with high temperatures (e.g., welding operations and exhaust from engines) gases will be formed.

Vapours

Vapours are the gaseous form of substances that normally are in the liquid or solid state at room temperature and normal pressure. When a liquid evaporates it changes to a gas and mixes with the surrounding air. A vapour can be regarded as a gas, where the maximal concentration of a vapour depends on the temperature and the saturation pressure of the substance. Any process involving combustion will generate vapours or gases. Degreasing operations might be performed by vapour phase degreasing or soak cleaning with solvents. Work activities like charging and mixing liquids, painting, spraying, cleaning and dry cleaning might generate harmful vapours.

Liquids

Liquids may consist of a pure substance or a solution of two or more substances (e.g., solvents, acids, alkalis). A liquid stored in an open container will partially evaporate into the gas phase. The concentration in the vapour phase at equilibrium depends on the vapour pressure of the substance, its concentration in the liquid phase, and the temperature. Operations or activities with liquids might give rise to splashes or other skin contact, besides harmful vapours.

Dusts

Dusts consist of inorganic and organic particles, which can be classified as inhalable, thoracic or respirable, depending on particle size. Most organic dusts have a biological origin. Inorganic dusts will be generated in mechanical processes like grinding, sawing, cutting, crushing, screening or sieving. Dusts may be dispersed when dusty material is handled or whirled up by air movements from traffic. Handling dry materials or powder by weighing, filling, charging, transporting and packing will generate dust, as will activities like insulation and cleaning work.

Fumes

Fumes are solid particles vaporized at high temperature and condensed to small particles. The vaporization is often accompanied by a chemical reaction such as oxidation. The single particles that make up a fume are extremely fine, usually less than 0.1 μm, and often aggregate in larger units. Examples are fumes from welding, plasma cutting and similar operations.

Mists

Mists are suspended liquid droplets generated by condensation from the gaseous state to the liquid state or by breaking up a liquid into a dispersed state by splashing, foaming or atomizing. Examples are oil mists from cutting and grinding operations, acid mists from electroplating, acid or alkali mists from pickling operations or paint spray mists from spraying operations.

 

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Contents

Occupational Hygiene References

Abraham, MH, GS Whiting, Y Alarie et al. 1990. Hydrogen bonding 12. A new QSAR for upper respiratory tract irritation by airborne chemicals in mice. Quant Struc Activity Relat 9:6-10.

Adkins, LE et al. 1990. Letter to the Editor. Appl Occup Environ Hyg 5(11):748-750.

Alarie, Y. 1981. Dose response analysis in animal studies: Prediction of human responses. Environ Health Persp 42:9-13.

American Conference of Governmental Industrial Hygienists (ACGIH). 1994. 1993-1994 Threshold Limit Values for Chemical Substances and Physical Agents and Biological Exposure Indices. Cincinnati: ACGIH.

—. 1995. Documentation of Threshold Limit Values. Cincinnati: ACGIH.

Baetjer, AM. 1980. The early days of industrial hygiene: Their contribution to current problems. Am Ind Hyg Assoc J 41:773-777.

Bailer, JC, EAC Crouch, R Shaikh, and D Spiegelman. 1988. One-hit models of carcinogenesis: Conservative or not? Risk Anal 8:485-490.

Bogers, M, LM Appelman, VJ Feron, et al. 1987. Effects of the exposure profile on the inhalation toxicity of carbon tetrachloride in male rats. J Appl Toxicol 7:185-191.

Boleij, JSM, E Buringh, D Heederik, and H Kromhour. 1995. Occupational Hygiene for Chemical and Biological Agents. Amsterdam: Elsevier.

Bouyer, J and D Hémon. 1993. Studying the performance of a job exposure matrix. Int J Epidemiol 22(6) Suppl. 2:S65-S71.

Bowditch, M, DK Drinker, P Drinker, HH Haggard, and A Hamilton. 1940. Code for safe concentrations of certain common toxic substances used in industry. J Ind Hyg Toxicol 22:251.

Burdorf, A. 1995. Certification of Occupational Hygienists—A Survey of Existing Schemes Throughout the World. Stockholm: International Occupational Hygiene Association (IOHA).

Bus, JS and JE Gibson. 1994. Body defense mechanisms to toxicant exposure. In Patty’s Industrial Hygiene and Toxicology, edited by RL Harris, L Cralley and LV Cralley. New York: Wiley.

Butterworth, BE and T Slaga. 1987. Nongenotoxic Mechanisms in Carcinogenesis: Banbury Report 25. Cold Spring Harbor, New York: Cold Spring Harbor Laboratory.

Calabrese, EJ. 1983. Principles of Animal Extrapolation. New York: Wiley.

Casarett, LJ. 1980. In Casarett and Doull’s Toxicology: The Basic Science of Poisons, edited by J Doull, CD Klaassen, and MO Amdur. New York: Macmillan.

Castleman, BI and GE Ziem. 1988. Corporate Influence on Threshold Limit Values. Am J Ind Med 13(5).

Checkoway, H and CH Rice. 1992. Time-weighted averages, peaks, and other indices of exposure in occupational epidemiolgy. Am J Ind Med 21:25-33.

Comité Européen de Normalisation (CEN). 1994. Workplace Atmoshperes—Guidance for the Assessment of Exposure to Chemical Agents for Comparison With Limit Values and Measurement Strategy. EN 689, prepared by CEN Technical Committee 137. Brussels: CEN.

Cook, WA. 1945. Maximum allowable concentrations of industrial contaminants. Ind Med 14(11):936-946.

—. 1986. Occupational Exposure Limits—Worldwide. Akron, Ohio: American Industrial Hygiene Association (AIHA).

Cooper, WC. 1973. Indicators of susceptibility to industrial chemicals. J Occup Med 15(4):355-359.

Corn, M. 1985. Strategies for air sampling. Scand J Work Environ Health 11:173-180.

Dinardi, SR. 1995. Calculation Methods for Industrial Hygiene. New York: Van Nostrand Reinhold.

Doull, J. 1994. The ACGIH Approach and Practice. Appl Occup Environ Hyg 9(1):23-24.

Dourson, MJ and JF Stara. 1983. Regulatory history and experimental support of uncertainty (safety) factors. Regul Toxicol Pharmacol 3:224-238.

Droz, PO. 1991. Quantification of concomitant biological and air monitoring results. Appl Ind Hyg 6:465-474.

—. 1992. Quantification of biological variability. Ann Occup Health 36:295-306.

Fieldner, AC, SH Katz, and SP Kenney. 1921. Gas Masks for Gases Met in Fighting Fires. Bulletin No. 248. Pittsburgh: USA Bureau of Mines.

Finklea, JA. 1988. Threshold limit values: A timely look. Am J Ind Med 14:211-212.

Finley, B, D Proctor, and DJ Paustenbach. 1992. An alternative to the USEPA’s proposed inhalation reference concentration for hexavalent and trivalent chromium. Regul Toxicol Pharmacol 16:161-176.

Fiserova-Bergerova, V. 1987. Development of using BEIs and their implementation. Appl Ind Hyg 2(2):87-92.

Flury, F and F Zernik. 1931. Schadliche Gase, Dampfe, Nebel, Rauch-und Staubarten. Berlin: Springer.

Goldberg, M, H Kromhout, P Guénel, AC Fletcher, M Gérin, DC Glass, D Heederik, T Kauppinen, and A Ponti. 1993. Job exposures matrices in industry. Int J Epidemiol 22(6) Suppl. 2:S10-S15.

Gressel, MG and JA Gideon. 1991. An overview of process hazard evaluation techniques. Am Ind Hyg Assoc J 52(4):158-163.

Henderson, Y and HH Haggard. 1943. Noxious Gases and the Principles of Respiration Influencing their Action. New York: Reinhold.

Hickey, JLS and PC Reist. 1979. Adjusting occupational exposure limits for moonlighting, overtime, and environmental exposures. Am Ind Hyg Assoc J 40:727-734.

Hodgson, JT and RD Jones. 1990. Mortality of a cohort of tin miners 1941-1986. Br J Ind Med 47:665-676.

Holzner, CL, RB Hirsh, and JB Perper. 1993. Managing workplace exposure information. Am Ind Hyg Assoc J 54(1):15-21.

Houba, R, D Heederik, G Doekes, and PEM van Run. 1996. Exposure sensitization relationship for alpha-amylase allergens in the baking industry. Am J Resp Crit Care Med 154(1):130-136.

International Congress on Occupational Health (ICOH). 1985. Invited lectures of the XXI International Congress on Occupational Health, Dublin. Scand J Work Environ Health 11(3):199-206.

Jacobs, RJ. 1992. Strategies to recognize biological agents in the work environment and possibilities for setting standards for biological agents. IOHA first International Science Conference, Brussels, Belgium 7-9 Dec 1992.

Jahr, J. 1974. Dose-response basis for setting a quartz threshold limit value. Arch Environ Health 9:338-340.

Kane, LE and Y Alarie. 1977. Sensory irritation to formaldehyde and acrolein during single and repeated exposures in mills. Am Ind Hyg Assoc J 38:509-522.

Kobert, R. 1912. The smallest amounts of noxious industrial gases which are toxic and the amounts which may perhaps be endured. Comp Pract Toxicol 5:45.

Kromhout, H, E Symanski, and SM Rappaport. 1993. Comprehensive evaluation of within-and between-worker components of occupational exposure to chemical agents. Ann Occup Hyg 37:253-270.

LaNier, ME. 1984. Threshold Limit Values: Discussion and 35 Year Index with Recommendations (TLVs: 1946-81). Cincinnati: ACGIH.

Lehmann, KB. 1886. Experimentelle Studien über den Einfluss Technisch und Hygienisch Wichtiger Gase und Dampfe auf Organismus: Ammoniak und Salzsauregas. Arch Hyg 5:1-12.

Lehmann, KB and F Flury. 1938. Toxikologie und Hygiene der Technischen Losungsmittel. Berlin: Springer.

Lehmann, KB and L Schmidt-Kehl. 1936. Die 13 Wichtigsten Chlorkohlenwasserstoffe der Fettreihe vom Standpunkt der Gewerbehygiene. Arch Hyg Bakteriol 116:131-268.

Leidel, NA, KA Busch, and JR Lynch. 1977. NIOSH Occupational Exposure Sampling Strategy Manuel. Washington, DC: NIOSH.

Leung, HW and DJ Paustenbach. 1988a. Setting occupational exposure limits for irritant organic acids and bases based on their equilibrium dissociation constants. Appl Ind Hyg 3:115-118.

—. 1988b. Application of pharmokinetics to derive biological exposure indexes from threshold limit values. Amer Ind Hyg Assoc J 49:445-450.

Leung, HW, FJ Murray and DJ Paustenbach. 1988. A proposed occupational exposure limit for 2, 3, 7, 8 - TCDD. Amer Ind Hyg Assoc J 49:466-474.

Lundberg, P. 1994. National and international approaches to occupational standard setting within Europe. Appl Occup Environ Hyg 9:25-27.

Lynch, JR. 1995. Measurement of worker exposure. In Patty’s Industrial Hygiene and Toxicology, edited by RL Harris, L Cralley, and LV Cralley. New York: Wiley.

Maslansky, CJ and SP Maslansky. 1993. Air Monitoring Instrumentation. New York: Van Nostrand Reinhold.

Menzel, DB. 1987. Physiological pharmacokinetic modelling. Environ Sci Technol 21:944-950.

Miller, FJ and JH Overton. 1989. Critical issues in intra-and interspecies dosimetry of ozone. In Atmospheric Ozone Research and Its Policy Implications, edited by T Schneider, SD Lee, GJR Wolters, and LD Grant. Amsterdam: Elsevier.

National Academy of Sciences (NAS) and National Research Council (NRC). 1983. Risk Assessment in the Federal Government: Managing the Process. Washington, DC: NAS.

National Safety Council (NSC). 1926. Final Report of the Committee of the Chemical and Rubber Sector on Benzene. Washington, DC: National Bureau of Casualty and Surety Underwriters.

Ness, SA. 1991. Air Monitoring for Toxic Exposures. New York: Van Nostrand Reinhold.

Nielsen, GD. 1991. Mechanisms of activation of the sensory irritant receptor. CRC Rev Toxicol 21:183-208.

Nollen, SD. 1981. The compressed workweek: Is it worth the effort? Ing Eng :58-63.

Nollen, SD and VH Martin. 1978. Alternative Work Schedules. Part 3: The Compressed Workweek. New York: AMACOM.

Olishifski, JB. 1988. Administrative and clinical aspects in the chapter Industrial Hygiene. In Occupational Medicine: Principles and Practical Applications, edited by C Zenz. Chicago: Year Book Medical.

Panett, B, D Coggon, and ED Acheson. 1985. Job exposure matrix for use in population based studies in England and Wales. Br J Ind Med 42:777-783.

Park, C and R Snee. 1983. Quantitative risk assessment: State of the art for carcinogenesis. Fund Appl Toxicol 3:320-333.

Patty, FA. 1949. Industrial Hygiene and Toxicology. Vol. II. New York: Wiley.

Paustenbach, DJ. 1990a. Health risk assesment and the practice of industrial hygiene. Am Ind Hyg Assoc J 51:339-351.

—. 1990b. Occupational exposure limits: Their critical role in preventative medicine and risk management. Am Ind Hyg Assoc J 51:A332-A336.

—. 1990c. What Does the Risk Assessment Process Tell us about the TLVs? Presented at the 1990 Joint Conference on Industrial Hygiene. Vancouver, BC, 24 October.

—. 1994. Occupational exposure limits, pharmacokinetics, and unusual workshifts. In Patty’s Industrial Hygiene and Toxicology. Vol. IIIa (4th edn.). New York:Wiley.

—. 1995. The practice of health risk assessment in the United States (1975-1995): How the US and other countries can benefit from that experience. Hum Ecol Risk Assess 1:29-79.

—. 1997. OSHA’s program for updating the permissible exposure limits (PELs): Can risk assessment help “move the ball forward”? Risk in Perspectives 5(1):1-6. Harvard University School of Public Health.

Paustenbach, DJ and RR Langner. 1986. Setting corporate exposure limits: State of the art. Am Ind Hyg Assoc J 47:809-818.

Peto, J, H Seidman, and IJ Selikoff. 1982. Mesothelioma mortality in asbestos workers: implications for models of carcinogenesis and risk assessment. Br J Cancer 45:124-134.

Phthisis Prevention Committee. 1916. Report of Miners. Johannesburg: Phthisis Prevention Committee.

Post, WK, D Heederik, H Kromhout, and D Kromhout. 1994. Occupational exposures estimated by a population specific job-exposure matrix and 25-year incidence rate of chronic non-specific lung disease (CNSLD): The Zutphen Study. Eur Resp J 7:1048-1055.

Ramazinni, B. 1700. De Morbis Atrificum Diatriba [Diseases of Workers]. Chicago: The Univ. of Chicago Press.

Rappaport, SM. 1985. Smoothing of exposure variability at the receptor: Implications for health standards. Ann Occup Hyg 29:201-214.

—. 1991. Assessment of long-term exposures to toxic substances in air. Ann Occup Hyg 35:61-121.

—. 1995. Interpreting levels of exposures to chemical agents. In Patty’s Industrial Hygiene and Toxicology, edited by RL Harris, L Cralley, and LV Cralley. New York: Wiley.

Rappaport, SM, E Symanski, JW Yager, and LL Kupper. 1995. The relationship between environmental monitoring and biological markers in exposure assessment. Environ Health Persp 103 Suppl. 3:49-53.

Renes, LE. 1978. The industrial hygiene survey and personel. In Patty’s Industrial Hygiene and Toxicology, edited by GD Clayton and FE Clayton. New York: Wiley.

Roach, SA. 1966. A more rational basis for air sampling programmes. Am Ind Hyg Assoc J 27:1-12.

—. 1977. A most rational basis for air sampling programmes. Am Ind Hyg Assoc J 20:67-84.

Roach, SA and SM Rappaport. 1990. But they are not thresholds: A critical analysis of the documentation of threshold limit values. Am J Ind Med 17:727-753.

Rodricks, JV, A Brett, and G Wrenn. 1987. Significant risk decisions in federal regulatory agencies. Regul Toxicol Pharmacol 7:307-320.

Rosen, G. 1993. PIMEX-combined use of air sampling instruments and video filming: Experience and results during six years of use. Appl Occup Environ Hyg 8(4).

Rylander, R. 1994. Causative agents for organic dust related disease: Proceedings of an international workshop, Sweden. Am J Ind Med 25:1-11.

Sayers, RR. 1927. Toxicology of gases and vapors. In International Critical Tables of Numerical Data, Physics, Chemistry and Toxicology. New York: McGraw-Hill.

Schrenk, HH. 1947. Interpretation of permissible limits. Am Ind Hyg Assoc Q 8:55-60.

Seiler, JP. 1977. Apparent and real thresholds: A study of two mutagens. In Progress in Genetic Toxicology, edited by D Scott, BA Bridges, and FH Sobels. New York: Elsevier Biomedical.

Seixas, NS, TG Robins, and M Becker. 1993. A novel approach to the characterization of cumulative exposure for the study of chronic occupational disease. Am J Epidemiol 137:463-471.

Smith, RG and JB Olishifski. 1988. Industrial toxicology. In Fundamentals of Industrial Hygiene, edited by JB Olishifski. Chicago: National Safety Council.

Smith, TJ. 1985. Development and application of a model for estimating alveolar and interstitial dust levels. Ann Occup Hyg 29:495-516.

—. 1987. Exposure assessment for occupational epidemiology. Am J Ind Med 12:249-268.

Smyth, HF. 1956. Improved communication: Hygienic standard for daily inhalation. Am Ind Hyg Assoc Q 17:129-185.

Stokinger, HE. 1970. Criteria and procedures for assessing the toxic responses to industrial chemicals. In Permissible Levels of Toxic Substances in the Working Environment. Geneva: ILO.

—. 1977. The case for carcinogen TLV’s continues strong. Occup Health Safety 46 (March-April):54-58.

—. 1981. Threshold limit values: Part I. Dang Prop Ind Mater Rep (May-June):8-13.

Stott, WT, RH Reitz, AM Schumann, and PG Watanabe. 1981. Genetic and nongenetic events in neoplasia. Food Cosmet Toxicol 19:567-576.

Suter, AH. 1993. Noise and conservation of hearing. In Hearing Conservation Manual. Milwaukee, Wisc: Council for Accreditation in Occupational Hearing Conservation.

Tait, K. 1992. The Workplace Exposure Assessment Expert System (WORK SPERT). Am Ind Hyg Assoc J 53(2):84-98.

Tarlau, ES. 1990. Industrial hygiene with no limits. A guest editorial. Am Ind Hyg Assoc J 51:A9-A10.

Travis, CC, SA Richter, EA Crouch, R Wilson, and E Wilson. 1987. Cancer risk management: A review of 132 federal regulatory decisions. Environ Sci Technol 21(5):415-420.

Watanabe, PG, RH Reitz, AM Schumann, MJ McKenna, and PJ Gehring. 1980. Implications of the mechanisms of tumorigenicity for risk assessment. In The Scientific Basis of Toxicity Assessment, edited by M Witschi. Amsterdam: Elsevier.

Wegman, DH, EA Eisen, SR Woskie, and X Hu. 1992. Measuring exposure for the epidemiologic study of acute effects. Am J Ind Med 21:77-89.

Weil, CS. 1972. Statistics versus safety factors and scientific judgment in the evaluation of safety for man. Toxicol Appl Pharmacol 21:454-463.

Wilkinson, CF. 1988. Being more realistic about chemical carcinogenesis. Environ Sci Technol 9:843-848.

Wong, O. 1987. An industry wide mortality study of chemical workers occupationally exposed to benzene. II Dose-response analyses. Br J Ind Med 44:382-395.

World Commission on Environment and Development (WCED). 1987. Our Common Future. Brundtland Report. Oxford: OUP.

World Health Organization (WHO). 1977. Methods used in Establishing Permissible Levels in Occupational Exposure to Harmful Agents. Technical Report No. 601. Geneva: International Labour Organization (ILO).

—. 1992a. Our Planet, Our Health. Report of the WHO Commission on Health and Environment. Geneva: WHO.

—. 1992b. Occupational Hygiene in Europe: Development of the Profession. European Occupational Health Series No. 3. Copenhagen: WHO Regional Office for Europe.

Zielhuis, RL and van der FW Kreek. 1979a. Calculations of a safety factor in setting health based permissible levels for occupational exposure. A proposal. I. Int Arch Occup Environ Health 42:191-201.

Ziem, GE and BI Castleman. 1989. Threshold limit values: Historical perspective and current practice. J Occup Med 13:910-918.