(BQ) Part 2 book “Current occupational and environmental medicine” has contents: Occupational mental health & workplace violence, occupational safety, disease surveillance, biologic monitoring, international chemicals policy, health, and human rights, outdoor air pollution, water pollution, multiple chemical sensitivity,… and other contents.
Section IV Occupational and Environmental Exposures 30 Metals Richard Lewis, MD, MPH Michael J Kosnett, MD, MPH The diverse physical properties of metals have resulted in their extensive use in industry These naturally occurring materials have long been recognized for their ability to impart a variety of valuable characteristics to finished goods Metals are used in the construction, automotive, aerospace, electronics, glass, and other manufacturing industries Metals are major sources of pigments and stabilizers for paints and plastics Metals are also used as catalysts and intermediates in the chemical and pharmaceutical industries Metals may be emitted as contaminants or by-products from industrial operations and power generation, and these have become the major sources of ongoing environmental contamination Metals are used rarely in their pure form, usually being present in alloys They also may be bound to organic materials, altering their physical characteristics and potential toxicity Some compounds, such as hydrides and carbonyls, are highly toxic and may be formed accidentally when the parent metal reacts with acids Metals may be altered by burning and smelting or after uptake by biologic systems The chemical structure of the metal or organometallic compound alters absorption, distribution, and toxicity Metals exert biologic effects chiefly through the formation of stable complexes with sulfhydryl groups, altering the structure and function of many proteins and enzyme systems Certain metals, such as zinc, chromium, and manganese, are essential for normal metabolism Others, such as lead, mercury, and arsenic, serve no recognized biologic purpose, raising public health concerns owing to their ubiquitous presence in living organisms Understanding and eliminating health risks from low-level background exposures remains a top priority in environmental health General population exposure to many metals is related primarily to air, water, and food contamination Background exposures vary considerably around the world owing to natural occurrence in soil and groundwater, as well as pollution from industrial operations, automotive exhaust, and power generation Familiarity with the potential health effects of metals in different settings is critical not only for the health and safety professional but also for the general medical practitioner ACUTE METAL TOXICITY Acute toxicity usually occurs after ingestion of metal-containing compounds or inhalation of high concentrations of metal dusts or fumes These can arise from improperly ventilated burning or welding operations or from unexpected chemical reactions Home remodeling activities can generate dust from paint pigments, particularly lead This and ingestion of paint chips (pica) are important causes of childhood poisoning Familiarity with the symptoms of acute heavy metal poisoning, along with an awareness of the potential sources of exposure, is critical for rapid detection and treatment The levels of most metals can be measured in blood or urine to confirm the diagnosis and guide therapy CHRONIC METAL TOXICITY Research into the health effects of low-level exposure to metals indicates that physiologic alterations occur at levels that have been considered safe previously The evidence for neurotoxicity, circulatory effects, nephrotoxicity, reproductive toxicity, and carcinogenicity at low levels of exposure continues to grow Regulatory agencies must consider these factors as they devise exposure standards that provide adequate margins of safety in protecting long-term population health The challenge for physicians is to differentiate global public health issues from specific clinical concerns in individual patients ARSENIC ESSENTIALS OF DIAGNOSIS Acute Effects • Gastrointestinal distress (nausea, vomiting, diarrhea, abdominal pain) • Hypotension, metabolic acidosis • Cardiopulmonary dysfunction (prolonged QT interval, arrhythmias, congestive cardiomyopathy, non-cardiogenic pulmonary edema) • Anemia and leukopenia • Sensorimotor peripheral neuropathy Chronic Effects • Constitutional (fatigue, malaise) • Anemia and leukopenia • Hyperkeratosis and hyperpigmentation • Sensorimotor peripheral neuropathy • Peripheral vascular disease • Cancer of the skin, lung, and bladder General Considerations Arsenic is a naturally occurring metalloid that occurs in a variety of chemical forms and valence states The elemental form, which seldom exists in nature and is of low solubility, is a rare cause of human toxicity Inorganic arsenic is encountered in commerce predominantly as the trivalent (As+3) or pentavalent (As+5) oxides, sulfides, or salts Trivalent forms generally have greater acute toxicity than the pentavalent species, but in vivo interconversion may occur, and compounds of both valences are capable of exerting a similar pattern of acute and chronic intoxication Organoarsenicals, which occur naturally and in many synthetic forms, vary widely in their toxicological attributes, from the virtually nontoxic natural compound arsenobetaine widely encountered in seafood, to the highly toxic vesicant warfare agent lewisite (dichloro [2-chlorovinyl] arsine) Arsine, a hydride gas (AsH3) is a potent hemolytic agent Use Arsenic is used principally in the United States in the production of chromated copper arsenide (CCA) wood preservatives for industrial applications (eg, marine timbers and utility poles); its widespread former use as a preservative for residential lumber was voluntarily discontinued in 2003 Arsenic is used a minor constituent of metal alloys, such as the hardening of lead in battery grids, bearings, and ammunition, and in the manufacture of certain types of glass With the exception of monosodium methanearsonate (MSMA) as an herbicide, virtually all the domestic use of arsenic as a pesticide or herbicide has been discontinued High purity arsenic is used in the manufacture of gallium arsenide chips and circuit boards incorporated in products in the electronics, aerospace, and telecommunications sectors Arsenic trioxide was introduced to the US Pharmacopoeia in 2000 as a drug for cancer chemotherapy Phenylarsenic compounds are used as feed additives for poultry and swine, and poultry litter marketed as a soil amendment may contain low levels of soluble arsenic Inorganic arsenic is occasionally encountered in folk remedies and tonics, particularly some of Asian origin Occupational & Environmental Exposure Occupational exposure to arsenic may occur in the smelting of lead, copper, gold, and other nonferrous metals Readily volatilized arsenic trioxide is concentrated in flue dust and can be condensed and recovered in a cooling chamber Furnace and flue maintenance operations carry risk of exposure Arsenic also may be found in fly and bottom ash from coal combustion, and exposure is possible during coal boiler maintenance In the microelectronics and glass industries, workers may be exposed to arsenic from source materials, finished products, or maintenance operations Arsine gas is used in semiconductor manufacturing and also may be formed accidentally when compounds or products containing inorganic arsenic come in contact with hydrogen or reducing agents in aqueous solution General population exposure to inorganic arsenic occurs primarily through ingestion of foodstuffs that contain arsenic as a consequence of its natural crustal occurrence or anthropogenic contamination In various parts of the world, inorganic arsenic of geologic origin may be found in artesian well water at concentrations that exceed the U.S Environmental Protection Agency (EPA) maximum contaminant level of 10 μg/L by one or more orders of magnitude Arsenic may also leach into groundwater from certain landfills or surface impoundments containing coal combustion waste Seafoods (fish, mollusks, and seaweeds) may often contain naturally occurring nontoxic organoarsenicals such as arsenobetaine or various arsenosugars Absorption, Metabolism, & Excretion Soluble arsenic compounds are well absorbed after ingestion or inhalation Percutaneous absorption is limited, but may be of clinical significance after extensive exposure to concentrated reagents Inorganic arsenic undergoes in vivo biomethylation to monomethylarsonic acid (MMA) and dimethylarsinic acid (DMA), which are predominantly excreted, together with residual inorganic arsenic, in the urine Approximately 10–30% appears in the urine as inorganic arsenic, 10–20% as MMA, and 60–70% as DMA Genetic, dietary, and dose factors appear to influence the extent of biomethylation, and a relatively higher percentage of MMA in the urine may reflect increased susceptibility to arsenic related disease When chronic daily absorption of inorganic arsenic is less than 1000 μg, approximately two-thirds of the absorbed dose is excreted in the urine within 2–3 days Arsenic binds to sulfhydryl groups present in keratinized tissue, and small amounts are excreted by incorporation into the hair and nails Arsenic compounds are believed to exert their hazardous effects through multiple modes of action, including inhibition of enzymes vital to cell metabolism, induction of oxidative stress, and alterations in gene expression and cell signal transduction Arsine gas uniquely induces massive hemolysis by forming a reactive intermediate with oxyhemoglobin that alters transmembrane ion flux Clinical Findings A Symptoms and Signs Acute exposure—Acute exposure to several hundred milligrams or more of a soluble inorganic arsenic salt may result in a constellation of multisystemic signs and symptoms that emerge over a period of hours to weeks Early prominent signs include gastrointestinal distress, including nausea, vomiting, diarrhea, and abdominal pain Diffuse capillary leak may result in hypotension, tachycardia, decreased urine output, and shock Central nervous system findings are highly variable, and range from none to seizures and encephalopathy If the patient survives the initial phase, a second phase within day to week may feature cardiac arrhythmias, congestive cardiomyopathy, and noncardiogenic pulmonary edema A third phase that emerges 1–4 weeks post ingestion may include anemia and leukopenia, and sensorimotor peripheral neuropathy Arsine gas is nonirritating, and inhalation yields no immediate symptoms A garlic-like odor is occasionally but not invariably noted After a dosedependent latent interval of 2–24 hours, massive hemolysis may ensue, accompanied by constitutional symptoms of headache, malaise, fever, chills, and gastrointestinal distress Hemoglobinuria imparts a reddish color to the urine, and elevated plasma hemoglobin may result in a bronze discoloration of the skin Oliguria and acute renal failure, which emerge within 1–3 days, are often major complications Subacute and chronic exposure—Subacute arsenic intoxication associated with absorption of weeks to months of >0.05 mg/kg/d may also result in multisystemic effects including fatigue, gastrointestinal symptoms, depressed hemoglobin, liver enzyme elevation, peripheral neuropathy, and prolonged QT interval, possibly associated with ventricular arrhythmias Chronic arsenic ingestion of >0.01 mg/kg/d over a period of years may result in the emergence of a distinctive pattern of spotted hyperpigmentation and palmarplantar hyperkeratosis, a sensory predominant peripheral neuropathy, vascular disease, and noncirrhotic portal hypertension Epidemiological data suggest a link between chronic arsenic ingestion and diabetes mellitus, hypertension, increased cardiovascular mortality, and nonmalignant respiratory disease Chronic arsenic inhalation may cause lung cancer, and chronic arsenic ingestion may cause cancer of the skin, lung, and bladder B Laboratory Findings Early in the phase of severe acute arsenic poisoning there may be laboratory evidence of metabolic acidosis and rhabdomyolysis As intoxication progresses, there may be anemia and leukopenia, hepatic transaminase elevation, and QT segment prolongation and arrhythmias on the electrocardiogram Measurement of urine arsenic is helpful in confirming recent exposure In the first to days following acute symptomatic arsenic intoxication, total urine arsenic concentration is typically ≫ 1000 μg/L and depending on the severity of poisoning may not return to back ground values for several weeks Ingestion of seafood, which may contain nontoxic organoarsenicals such as arsenobetaine and arsenosugars, may greatly elevate total urine arsenic concentration for up to days It may sometimes be useful to have urine arsenic reported as inorganic arsenic plus its primary human metabolites MMA and DMA—the sum of these three species is usually less than 20 μg/L in the general population from background dietary and environmental exposure Segmental analysis of arsenic in the hair and nails may sometimes offer forensic evidence of elevated arsenic exposure months after urine arsenic concentration has normalized, but values should be interpreted cautiously owing to the potential of external contamination Blood arsenic, which has a highly variable relationship to exposure and is subject to rapid clearance, is rarely of value for clinical diagnosis or biological monitoring Prevention Because arsenic is a known human carcinogen, workplace exposure should be reduced as much as feasible by a program of engineering and administrative controls, and personal protective equipment Biological monitoring of arsenic in urine may yield information on recent airborne or inhalation exposure to soluble arsenic compounds, but may have limited utility after inhalation of poorly soluble arsenic aerosols Treatment Management of acute arsenic intoxication should combine intensive supportive care of metabolic acidosis, hypotension, and other cardiovascular derangements with prompt administration of chelating agents Intravenous unithiol (DMPS), the chelating agent of choice, may be of limited availability in the United States Other useful agents include intramuscular dimercaprol and oral succimer (DMSA) Gastric contamination can be considered Prolonged inpatient support and monitoring may be indicated for initially symptomatic patients due to delayed cardiopulmonary and neurologic complications Management of chronic arsenic intoxication should focus on removal from sources of exposure and supportive care Oral chelation with succimer can be considered in individuals with high urine arsenic concentrations, as may folate supplementation in deficient individuals Treatment of arsine gas poisoning should focus on vigorous intravenous hydration, possibly supplemented by osmotic diuresis with mannitol, to maintain urine output and reduce the acute risk of hemoglobinuric renal failure Elevation of plasma or serum hemoglobin levels of 1.5 g/dL or higher, and/or signs of renal insufficiency should prompt exchange transfusion with whole blood Hemodialysis may be indicated for renal failure, but is not a substitute for the exchange transfusion-mediated removal of the arsenic-hemoprotein complexes thought to contribute to ongoing hemolysis Chelation is of uncertain value in the management of arsine intoxication BERYLLIUM ESSENTIALS OF DIAGNOSIS Tracheobronchitis, pneumonitis Granulomatous pulmonary disease Dermatitis (ulceration and granulomas) Eye, nose, and throat irritation Lung cancer General Considerations Beryllium is a lightweight gray metal with high tensile strength It is extracted from beryl ore after grinding and heating using electrolytic reduction Bertrandite (4BeO·2SiO2·H2O), although lower in beryllium content (0.1–3%), provides a source of acid-soluble beryllium that is more easily extracted Use The unique properties of beryllium are ideally suited for the production of hard, corrosion-resistant alloys for use in the aerospace industry Beryllium alloys (primarily copper) are used in tools, bushings, bearings, and electronic components Beryllium is used in nuclear reactors as a neutron moderator and a fuel source Beryllium oxide combines high thermal conductivity with high electrical resistance for use in ceramics, microwave tubes, and semiconductors Beryllium had been used historically in the manufacture of fluorescent and neon lamps, leading to numerous cases of beryllium disease Occupational & Environmental Exposure The health risks from exposure to beryllium vary based on the purity of the material and the particle size Mining of beryl ore appears to result in a relatively low risk of berylliosis In contrast, the purification and use of refined beryllium compounds, particularly beryllium oxide, continues to result in a substantial risk of sensitization and disease The aerospace, nuclear, electronics, and beryllium alloy industries continue to search for methods of providing adequate worker protection Exposure to minute, ultrafine particles, rather than total mass, may be the key factor in exposure and sensitization Assessment and control of beryllium exposure remain challenging Current exposure limits may not be adequate, with the most recent ACGIH recommendations being 40-fold lower than the OSHA PEL and 10 times less than the NIOSH REL Absorption, Metabolism, & Excretion Beryllium compounds are poorly absorbed after inhalation, ingestion, or skin contact Beryllium may be retained in the lung or deposited in bone, liver, and spleen Renal excretion is slow but may be used to confirm exposure because levels usually are not detectable in nonexposed individuals The development of berylliosis does not have a clear dose-response, suggesting that particle size and individual sensitivity are the key factors for both sensitization and disease development Pathologically, beryllium toxicity is a systemic disease evidenced by the presence of noncaseating granulomas in numerous tissues, including lung, liver, skin, and lymph nodes Clinical Findings A Symptoms and Signs Acute or subacute exposure—Acute or subacute exposure to beryllium blood tests for TB, 314 serologic, hepatitis B, 317t tuberculin skin, 313–314 “two-step” method, for tuberculosis, 313–314 unproven and inappropriate, 257, 258t 1,1,2,2-Tetrachloro-2,2-difluoroethane, properties, odor thresholds, exposure limits, 527t 2,3,7,8-Tetrachlorodibenzo-p -dioxin (2,3,7,8-TCDD) environmental exposure, 518 mechanism of action, 518 occupational exposure, 518 uses, 517–518 Tetrachloroethane, 752t, 753t acute renal dysfunction and, 417 hepatotoxicity, 397t, 398 1,1,2,2-Tetrachloroethane, properties, odor thresholds, exposure limits, 527t Tetrachloroethylene, 721t acute hepatic injury and, 401 Tetracycline, 399 Tetrahydrocannabinol (THC), 632 Tetrahydrofuran, 721t properties, odor thresholds, exposure limits, 528t Tetronic acid derivatives, as insecticides, 602 Texas, workers’ compensation in, 47 Textile industry, laryngeal cancer in, 296 Thallium differential diagnosis, 479 metabolism, 478 neurologic manifestations, 433t occupational and environmental exposure, 478 in toxic polyneuropathy, 428t uses, 478 Therapeutic mutagens, leukemia and, 270 Therapies, unproven and inappropriate, 257, 258t Thermal burns of eye and eyelid, 142 skin disorder and, 342 Thermal comfort zone, 218f Thessaly test, 111t, 113 Thiacloprid, 598t Thiamethoxam, 598t Thiocarbamate compounds, 610–611 Thiophanate methyl, 453t Thiram, 610t Thiuram allergy, 332t Thoracentesis, mesothelioma and, 294 Thoracic outlet syndrome, 77 Thoracoscopy, mesothelioma and, 294 Thoracotomy, mesothelioma and, 294 Thorium, hearing loss and, 166 Threshold Limit Values (TLVs) industrial hygiene and, 676 for lifting, 212–213 for noise, 216f for solvents, 525t–528t Thresholds, in carcinogenesis, 278–279 Thrombocytopenia, toxic, 273–274, 273t Tick-borne diseases, 312 Tin, occupational exposure to, 378 Tixocortol, 332t TLVs See Threshold Limit Values TMA See Trimellitic anhydride TMA flu, 253 TNT See Trinitrotoluene Tobacco, chewing, 301 Tobacco smoke See Cigarette smoking Tobacco workers, allergens and, 246t TOC See Total organic carbon Toluene, 722t, 751t, 752t acute renal failure and, 417 exposure limits, 570 hearing loss and, 166 neurologic manifestations, 433t properties, odor thresholds, exposure limits, 525t reproductive effects, 537 Toluene diamine, adverse male reproductive effects, 457t Toluene diisocyanate (TDI), 722t irritant effect, 253 thrombocytopenia and, 273, 273t Toluidine, methemoglobinemia/oxidative hemolysis and, 262t o -Toluidine, uses, 495 Tool handles, proper design, 207–208 Total organic carbon (TOC), 804–805 Total suspended solids (TSSs), 804–805 Toxic agents/materials absorption, 227–228 bioavailability, 227 cellular membrane permeability and, 227–228 chemical structure, 223 classification of, 223, 226 clearance, 229 distribution, 228 dose-response curves and, 230–232, 230f, 231f effects, 223, 226 onset, 226 reversibility, 226 tests, 229 elimination of, 233 environmental factors and, 226 excretion, 228–229 exposure, duration, frequency, and route, 226 to female reproductive system, 440t gastrointestinal absorption, 227 high- vs low-dose exposure to, 232 in lactation, 439 mechanism of action, 226 medium, 223 metabolism, 228 physical state, 223 pulmonary absorption of, 227 responses to, 226 site of injury by, 226 size of, 223 susceptibility, 226 volume of distribution, 229 Toxic cataracts, 149 Toxic inhalation injury, 364–367, 366t, 783–784 Toxic polyneuropathies, 427–429, 428t Toxic thrombocytopenia, 273–274, 273t Toxicant-associated steatohepatitis (TASH), 402 Toxicity, tests for, 229 Toxicodynamics, 227–229 Toxicokinetics, 227–229 Toxicologic risk assessment, 229–230 Toxicology, 223–233 cardiovascular, 386–394 dose-response curves in, 230–232, 230f, 231f female reproductive, 436–448 liver, 396–414 male reproductive, 450–462 exposure assessment, 454–455 management of toxic effects, 233 neurotoxicology, 425–434 renal, 415–423 Toxics Release Inventory (TRI), 750–753, 751t–752t, 756 Toxins, 644–651 botulinum, 649–650 ricin, 650–651 Trackball, position of, 206 Training lack of, in occupational medicine, in occupational health nursing, in occupational medicine, Trauma hearing loss from, 165–166 noise-induced hearing loss and, 161 Traumatic cataracts, 148 Traumative irritant dermatitis, 325 Travel, infectious diseases associated with, 318 Traveler’s diarrhea, prophylaxis, for traveling, 319–320 Trench foot, 173 TRI (toxics release inventory), 750–753, 751t–752t, 756 Triadimefon, 453t Triangular fibrocartilage complex tears, 91 Triazole compounds, 610t, 611 Trichlorion, lethal dose, 584t Trichloroacetic acid, 720t, 722t Trichloroethane acute hepatic injury and, 401 neurological disorders caused by, 433t occupational exposure, 553 1,1,1-Trichloroethane, 720t 1,1,2-Trichloroethane, properties, odor thresholds, exposure limits, 527t Trichloroethanol, 720t Trichloroethylene, 722t, 752t, 753t occupational exposure, 552–553 occupational liver disease and, 397t peripheral neuropathy and, 532 properties, odor thresholds, exposure limits, 527t in toxic polyneuropathy, 428t Trichloroethylene, acute renal dysfunction and, 417 Trichlorofluoromethane, properties, odor thresholds, exposure limits, 527t Triclosan, 714t Triethylamine, properties, odor thresholds, exposure limits, 527t Trifloxystrobin, 610t Trifluralin, 613t Trigeminal nerve anesthesia, trichloroethylene and, 532 Trigger digit, 86–87 Trigger finger/thumb, 207 Trimellitic anhydride (TMA), 245, 248 immediate-type reaction, 253 irritant respiratory syndrome and, 254 occupational asthma and, 373t pulmonary disease-anemia syndrome and, 254 Trimethylamine, properties, odor thresholds, exposure limits, 527t Trinitrotoluene (TNT) aplastic anemia and, 271, 272t hepatotoxicity, 397t, 398 methemoglobinemia/oxidative hemolysis and, 262t Triphenyltin, 610t Tropical acne, 337 T.R.U.E Test, 331, 332, 332t TSSs See Total suspended solids t -test, 846–849 paired, 848–849 TTS See Temporary threshold shift Tubercle bacilli, 313 Tuberculin skin test, 313–314 Tuberculosis, 313–315 bovine, 339 control and treatment, 314–315 incidence, 313 silicosis and, 379 of skin, 339 tests blood, 314 tuberculin skin test, 313–314 “two-step” method, 313–314, 314f Tularemia, 312 in biological warfare, 648–649 Tumor development, stages, 276–278, 277f Tungsten carbide, 377 Tunica albuginea, 452f Tuning fork tests, 152 Turpentine occupational exposure, 555 properties, odor thresholds, expo, sure limits, 528t thrombocytopenia and, 273, 273t Twisting, 210f Tympanometry, 152 impedence, 359t Typhoidal tularemia, 649 U UDGA See Urinary D-glucaric acid, liver function and Ulceroglandular disease, 649 Ulnar collateral ligament injury, 79t of the thumb, 90–91 Ulnar fractures, 94 Ulnar nerve entrapment at elbow, 79t, 81–82, 81f Ulnar neuropathy at wrist, 88–89 Ultraviolet (UV) radiation and eye injuries, 148 injuries caused by, 184–186, 184t occupational skin cancer and, 338 skin cancer and, 300 in welding, 482t workers exposed to, 184t Umbilical cord blood, biological monitoring of, 712 Undulant fever See Brucellosis United Kingdom, workers’ compensation history in, 40 United States employment, illness/chronic diseases associated with farm work in, 23t international migrant workers in, 20t, 21, 21t United States, workers’ compensation history in, 41 University of Pennsylvania Smell Identification Test (UPSIT), 360 Unproven practices, 257, 258t Uracil mustard, 453t Uranium, 722t chronic kidney disease and, 422 Urea nitrogen, blood, 415 Urinary D-glucaric acid (UDGA), liver function and, 411–412 Urine biological monitoring of, 712–713 fate of nonpersistent chemical in, 713f–714f Urine bilirubin, liver disease and, 410 Uroporphyrin III, 265 Urticaria contact, 336–337, 336f heat (cholinergic), 179 immunologic (allergic) contact, 336 nonimmunologic (nonallergic) contact, 326, 336 UV radiation See Ultraviolet radiation V Vaccines See also Immunization hepatitis B, 316, 405–407 travel, 318–320 yellow fever, 319 Vacor, 428t Valgus stress test, 109f, 112 Validity of claims, 47 Valley fever, 311 p -value, 851–852 Vanadium, occupational exposure, 481 Vapor contaminants, sampling of, 669–671 Vapor(s), definition, 558t Varus stress test, 110f, 112 Vas deferens, 452f VDTs See Video display terminals Vegetable dusts, occupational asthma and, 372 Vegetable products, occupational hypersensitivity disorders and, 252–253 Vehicle operators, vibration and, 219 Ventricular fibrillation, hypothermia and, 171 Vibration, 199t disorders caused by, 193–194 prevention of occupational injury and, 218–219 vision and, 219 whole-body, 214f, 219 Vibration-induced white finger disease, 193–194, 219 Vibration syndrome, 342 of hand arm, 89–90 Video display terminals (VDTs) adverse female reproductive effects and, 440t occupational skin disorders and, 342 use, effects of, 149 Vinyl acetate, 752t Vinyl chloride acquired porphyria and, 267–268 adverse male reproductive effects, 457t liver cancer and, 298, 299, 397t thrombocytopenia and, 273, 273t Vinyl chloride disease, 521 Vinyl chloride monomer, 520–522 environmental exposure, 520 mechanism of action, 520 occupational exposure, 520 Vinylidene chloride, acute renal dysfunction and, 417 Violence, workplace, 42 Viral skin diseases, 340 Viral warts, 340 Viruses, flu, 310 Visible radiation, injuries from, 183–184 Vision 20/20, 139 vibration and, 219 Visual acuity, 137 test of, 139–140, 140f Visual fields, test of, 140 Vitamin B12, deficiency, nitrous oxide exposure and, 432 Vitreous, 136f Vocal cord dysfunction (VCD), 358 Vocational rehabilitation, 43, 57–58 Volatile organic compounds (VOCs), 671, 794–795 Volatility, solvents and, 524 Vortex vein, 136f W Walk-through survey, 666 Warfarin, as rodenticide, 608–609, 608t Warmup, or work in cold, 170t Warts necrogenic, 339 Prosector’s, 339 viral, 340 Wastewater treatment, 805–806 Water pollution, 803–817 microbiologic control of, 804–806 regulatory considerations for, 816–817 Water-insoluble airborne intoxicants, 563–564 Water-soluble airborne toxicants, 563 Weber test, 152 Weighting scale adjustment, to noise reduction rating, 163 Welder’s flash, 145, 185, 482–484 Welding adverse male reproductive effects, 457t air contaminants, 482t coating and contaminants in, 483t health hazards, 482–483, 482t Wheat weevil lung, 373t Whirlpool therapy, for frostbite, 174 White finger disease, vibration induced, 193–194, 219 Whitewashing, 265 Whole-body vibration, 214f, 219 Wholly administrative system, for claims disputes, 48 Wind chill index, 170 Wipe sampling, 673, 673f Women body dimensions, 202f reach limits, 203 reproductive toxicology (See Female reproductive toxicology) Wood dusts allergy, 253 nasal and sinus cancer and, 295 occupational asthma and, 372–373 Wool alcohol allergy, 332t Word recognition score (WRS), 152 Work absence from, and disability, 51 outdoors, warm-up schedule for, 170t return to blue flags, 55t delayed, 52–54 early, 45 Work capacity, estimating, 214–215, 215t Work practices, 674–675 Work restrictions, 45 Worker(s) body size, cart handle designs and, 211f chemical exposures to, migrants, 19–24 health profiles, 23 noise education for, 162 personal protection, 679 trafficking of, 20–21, 23–24 work-related pathogens infections, 309t–310t Workers, biomonitoring of, 724 Workers’ compensation, 2, 40–49 benefit types, 42–44 characteristics of, 41–44 apportionment, 44 benefits, 42–44 causation test, 41–42 compromise and release settlements, 44 experience rating, 44 no-fault principle and exclusive remedy, 41 claims disputes, 47–48 cost of, 46–47 deficiencies in, 40 demonstration of ability to pay, 46–47 employers’ responsibilities, 46–49 ethical consideration and, 708 exempt employees, 46 hearing loss, 167 law, 40 penalties for lack of, 47 percent of workforce covered, 46 physician choice and, 45 role of physician in, 44–46 Social Security and, 40 validity of claims, 47 Workers’ compensation board, in claims disputes, 48 Working conditions, worldwide, Workplace assessment, 27–28 health hazards in anticipation, 665 control model of, 678f evaluation, 666–668 identification, 665–666 violence, 42, 626–628, 626t trauma intervention, 627–628 violence prevention, 627 warning behaviors, 626–627, 627t Workstations computer, 205–206, 205f design, 200–205 World Health Organization (WHO), Wrist injuries of, 84–94 osteoarthritis of, 92–93 pain, 84 sprain of, 90 WRS See Word recognition score X Xenobiotics end-stage renal disease and, 423 hepatic metabolism, 399 X-ray(s), and radiation exposure, 186 Xylene(s), 752t properties, odor thresholds, exposure limits, 525t Y Yellow fever occupational liver disease and, 408 travel and, 319 Yersinia pestis, as biological warfare agent, 647–648 Yu-cheng, 511 Yusho, 511 Z Zinc, neurologic manifestations, 434 Zinc chloride, 569 Zinc phosphide, 604t Zinc protoporphyrin (ZPP), 719t Zineb, 610t Zing phosphide, 608t Ziram, lethal dose, 610t Zonule, 136f Zoonoses, 320 ... rectifiers and semiconductors Occupational & Environmental Exposure Workers engaged in the refining of copper and silver may be exposed to airborne selenium and tellurium fumes and dust Selenium and. .. adverse health effects, and periodic worker education regarding the nature of lead hazards and controls In 20 12, CDC recommended parental education, environmental investigation, and additional medical... dyeing, and as a colorant in ceramics and glass Organic vanadium compounds are used as catalysts and coatings Occupational & Environmental Exposure Exposure to vanadium pentoxide dusts and fumes